Minoxidil - Revision history

Dmitry Dzhagarov: /* Application for hair growth */

2024-03-14T03:36:56Z

Application for hair growth

← Older revision		Revision as of 03:36, 14 March 2024
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	After minoxidil was was approved and marketed for the treatment of hypertension, clinicians learned that the drug stimulated hair growth.<ref>Zappacosta, A. R. (1980). Reversal of baldness in patient receiving minoxidil for hypertension. The New England Journal of Medicine, 303(25), 1480-1481. PMID: 7432414 DOI: 10.1056/nejm198012183032516</ref><ref>Suchonwanit, P., Thammarucha, S., & Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug design, development and therapy, 2777-2786. PMID: 31496654 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/ PMC6691938] DOI: 10.2147/DDDT.S214907</ref>		After minoxidil was was approved and marketed for the treatment of hypertension, clinicians learned that the drug stimulated hair growth.<ref>Zappacosta, A. R. (1980). Reversal of baldness in patient receiving minoxidil for hypertension. The New England Journal of Medicine, 303(25), 1480-1481. PMID: 7432414 DOI: 10.1056/nejm198012183032516</ref><ref>Suchonwanit, P., Thammarucha, S., & Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug design, development and therapy, 2777-2786. PMID: 31496654 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/ PMC6691938] DOI: 10.2147/DDDT.S214907</ref>
	<ref>Song, D., Pan, S., Jin, W., Wu, R., Zhao, T., Jiang, J., & Zhu, M. (2023). Minoxidil delivered via a stem cell membrane delivery controlled release system promotes hair growth in C57BL/6J mice. Frontiers in Bioengineering and Biotechnology, 11. PMID: 38260729 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10800965/ PMC10800965] DOI: 10.3389/fbioe.2023.1331754</ref> The mechanism of action of minoxidil on hair growth is probably not related to its effect on blood pressure in the vessels, since increased hair growth is observed even with very low doses of the drug (<5-mg/day) that do not cause a noticeable decrease in blood pressure.<ref>Ong, M., Do, H., Ho, B., & Lipner, S. R. (2024). Low-dose oral minoxidil for androgenetic alopecia is not associated with clinically significant blood-pressure changes: A retrospective study. Journal of the American Academy of Dermatology, 90(2), 425-427. PMID: 37839733 [https://doi.org/10.1016/j.jaad.2023.10.010 DOI: 10.1016/j.jaad.2023.10.010]</ref> Moreover, oral administration of the drug, even in such small doses, turned out to be a more effective way to stimulate hair growth than applying it to the skin.		<ref>Song, D., Pan, S., Jin, W., Wu, R., Zhao, T., Jiang, J., & Zhu, M. (2023). Minoxidil delivered via a stem cell membrane delivery controlled release system promotes hair growth in C57BL/6J mice. Frontiers in Bioengineering and Biotechnology, 11. PMID: 38260729 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10800965/ PMC10800965] DOI: 10.3389/fbioe.2023.1331754</ref> The mechanism of action of minoxidil on hair growth is probably not related to its effect on blood pressure in the vessels, since increased hair growth is observed even with very low doses of the drug (<5-mg/day) that do not cause a noticeable decrease in blood pressure.<ref>Ong, M., Do, H., Ho, B., & Lipner, S. R. (2024). Low-dose oral minoxidil for androgenetic alopecia is not associated with clinically significant blood-pressure changes: A retrospective study. Journal of the American Academy of Dermatology, 90(2), 425-427. PMID: 37839733 [https://doi.org/10.1016/j.jaad.2023.10.010 DOI: 10.1016/j.jaad.2023.10.010]</ref> Moreover, oral administration of the drug, even in such small doses, turned out to be a more effective way to stimulate hair growth than applying it to the skin.

			In hair follicles (HFs), minoxidil is converted to its active form, minoxidil sulphate, by the SULT1A1 sulfotransferase enzyme found in the outer root sheath (ORS). Individuals with loss-of-function mutations in the SULT1A1 gene have been referred to as non-responders to minoxidil.<ref>Roberts, J., Desai, N., McCoy, J., & Goren, A. (2014). Sulfotransferase activity in plucked hair follicles predicts response to topical minoxidil in the treatment of female androgenetic alopecia. Dermatologic Therapy, 27(4), 252-254. PMID: 24773771 DOI: 10.1111/dth.12130</ref><ref>PMID: 35950120 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9326921/ PMC9326921] DOI: 10.5114/ada.2020.99947</ref>

	== References ==		== References ==

Dmitry Dzhagarov: /* Application for stimulation of elastin expression */

2024-02-16T19:33:44Z

Application for stimulation of elastin expression

← Older revision		Revision as of 19:33, 16 February 2024
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	'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Rønnow, S. R., Kristensen, J. H., Thorlacius-Ussing, J., Karsdal, M. A., & Heinz, A. (2024). Elastin. In Biochemistry of Collagens, Laminins and Elastin (pp. 279-289). Academic Press. https://doi.org/10.1016/B978-0-443-15617-5.00016-0</ref><ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>		'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Rønnow, S. R., Kristensen, J. H., Thorlacius-Ussing, J., Karsdal, M. A., & Heinz, A. (2024). Elastin. In Biochemistry of Collagens, Laminins and Elastin (pp. 279-289). Academic Press. https://doi.org/10.1016/B978-0-443-15617-5.00016-0</ref><ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>
	Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />		Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />

			When treating fibrosis and for activation of elastin synthesis, '''oral doses of minoxidil should be used not exceeding 1.25 - 2.5 mg per day.'''

	== Treatment of fibrosis ==		== Treatment of fibrosis ==

Dmitry Dzhagarov: /* Treatment of pulmonary fibrosis */

2024-02-06T12:54:51Z

Treatment of pulmonary fibrosis

← Older revision		Revision as of 12:54, 6 February 2024
Line 6:		Line 6:
	Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />		Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />

	== Treatment of ~~pulmonary~~ fibrosis ==		== Treatment of fibrosis ==
	Lysyl hydroxylase modify and crosslink proteins by converting lysine to hydroxylysine and so make collagen more resistant to degradation.<ref>Van Der Slot, A. J., Zuurmond, A. M., Van Den Bogaerdt, A. J., Ulrich, M. M., Middelkoop, E., Boers, W., ... & Bank, R. A. (2004). Increased formation of pyridinoline cross-links due to higher telopeptide lysyl hydroxylase levels is a general fibrotic phenomenon. Matrix biology, 23(4), 251-257.</ref> Minoxidil was reported to reduce lysyl hydroxylase activity by decreasing the lysine hydroxylase mRNA level.<ref>Hautala, T., Heikkinen, J., Kivirikko, K. I., & Myllylä, R. (1992). Minoxidil specifically decreases the expression of lysine hydroxylase in cultured human skin fibroblasts. Biochemical Journal, 283(1), 51-54.</ref><ref>Zuurmond, A. M., van der Slot-Verhoeven, A. J., van Dura, E. A., De Groot, J., & Bank, R. A. (2005). Minoxidil exerts different inhibitory effects on gene expression of lysyl hydroxylase 1, 2, and 3: implications for collagen cross-linking and treatment of fibrosis. Matrix biology, 24(4), 261-270.</ref> and thus reducing the formation of hydroxyallysine cross-links.<ref name="hydroxylase" >Shao, S., Zhang, X., Duan, L., Fang, H., Rao, S., Liu, W., ... & Zhang, X. (2018). Lysyl hydroxylase inhibition by minoxidil blocks collagen deposition and prevents pulmonary fibrosis via TGF-β1/Smad3 signaling pathway. Medical science monitor: international medical journal of experimental and clinical research, 24, 8592.PMID: 30481795 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278642/ PMC6278642] DOI: 10.12659/MSM.910761</ref> Thus minoxidil exert anti-fibrotic properties. However, these reducing effects of minoxidil on the pulmonary fibrosis were at least partly mediated via inhibition of the matrix metalloproteinases and TGF-β1/Smad3 signaling.<ref name="hydroxylase" />		Lysyl hydroxylase modify and crosslink proteins by converting lysine to hydroxylysine and so make collagen more resistant to degradation.<ref>Van Der Slot, A. J., Zuurmond, A. M., Van Den Bogaerdt, A. J., Ulrich, M. M., Middelkoop, E., Boers, W., ... & Bank, R. A. (2004). Increased formation of pyridinoline cross-links due to higher telopeptide lysyl hydroxylase levels is a general fibrotic phenomenon. Matrix biology, 23(4), 251-257.</ref> Minoxidil was reported to reduce lysyl hydroxylase activity by decreasing the lysine hydroxylase mRNA level.<ref>Hautala, T., Heikkinen, J., Kivirikko, K. I., & Myllylä, R. (1992). Minoxidil specifically decreases the expression of lysine hydroxylase in cultured human skin fibroblasts. Biochemical Journal, 283(1), 51-54.</ref><ref>Zuurmond, A. M., van der Slot-Verhoeven, A. J., van Dura, E. A., De Groot, J., & Bank, R. A. (2005). Minoxidil exerts different inhibitory effects on gene expression of lysyl hydroxylase 1, 2, and 3: implications for collagen cross-linking and treatment of fibrosis. Matrix biology, 24(4), 261-270.</ref> and thus reducing the formation of hydroxyallysine cross-links.<ref name="hydroxylase" >Shao, S., Zhang, X., Duan, L., Fang, H., Rao, S., Liu, W., ... & Zhang, X. (2018). Lysyl hydroxylase inhibition by minoxidil blocks collagen deposition and prevents pulmonary fibrosis via TGF-β1/Smad3 signaling pathway. Medical science monitor: international medical journal of experimental and clinical research, 24, 8592.PMID: 30481795 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278642/ PMC6278642] DOI: 10.12659/MSM.910761</ref> Thus minoxidil exert anti-fibrotic properties. However, these reducing effects of minoxidil on the pulmonary fibrosis were at least partly mediated via inhibition of the matrix metalloproteinases and TGF-β1/Smad3 signaling.<ref name="hydroxylase" />

	== Application for hair growth ==		== Application for hair growth ==

Dmitry Dzhagarov at 12:04, 6 February 2024

2024-02-06T12:04:10Z

← Older revision		Revision as of 12:04, 6 February 2024
Line 1:		Line 1:
	'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906.</ref> Oral minoxidil was FDA-approved for treatment of hypertension in 1979. Off-label low-dose oral minoxidil (≤5-mg/day) has been studied for androgenetic alopecia treatment.<ref>Randolph, M., & Tosti, A. (2021). Oral minoxidil treatment for hair loss: A review of efficacy and safety. Journal of the American Academy of Dermatology, 84(3), 737-746 PMID: 32622136 DOI: 10.1016/j.jaad.2020.06.1009</ref>		'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906.</ref> Oral minoxidil was FDA-approved for treatment of hypertension in 1979.<ref>Zins, G. R. (1988). The history of the development of minoxidil. Clinics in dermatology, 6(4), 132-147.</ref> Off-label low-dose oral minoxidil (≤5-mg/day) has been studied for androgenetic alopecia treatment.<ref>Randolph, M., & Tosti, A. (2021). Oral minoxidil treatment for hair loss: A review of efficacy and safety. Journal of the American Academy of Dermatology, 84(3), 737-746 PMID: 32622136 DOI: 10.1016/j.jaad.2020.06.1009</ref>

	== Application for stimulation of elastin expression ==		== Application for stimulation of elastin expression ==

Dmitry Dzhagarov at 11:50, 6 February 2024

2024-02-06T11:50:44Z

← Older revision		Revision as of 11:50, 6 February 2024
Line 1:		Line 1:
	'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906.</ref> Oral minoxidil was FDA-approved for treatment of hypertension in 1979. Off-label low-dose oral minoxidil (≤5-mg/day) has been studied for androgenetic alopecia treatment,<ref>Randolph, M., & Tosti, A. (2021). Oral minoxidil treatment for hair loss: A review of efficacy and safety. Journal of the American Academy of Dermatology, 84(3), 737-746 PMID: 32622136 DOI: 10.1016/j.jaad.2020.06.1009</ref> ~~and~~		'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906.</ref> Oral minoxidil was FDA-approved for treatment of hypertension in 1979. Off-label low-dose oral minoxidil (≤5-mg/day) has been studied for androgenetic alopecia treatment.<ref>Randolph, M., & Tosti, A. (2021). Oral minoxidil treatment for hair loss: A review of efficacy and safety. Journal of the American Academy of Dermatology, 84(3), 737-746 PMID: 32622136 DOI: 10.1016/j.jaad.2020.06.1009</ref>

	== Application for stimulation of elastin expression ==		== Application for stimulation of elastin expression ==

Dmitry Dzhagarov at 11:49, 6 February 2024

2024-02-06T11:49:24Z

← Older revision		Revision as of 11:49, 6 February 2024
Line 1:		Line 1:
	'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906.</ref>		'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906.</ref> Oral minoxidil was FDA-approved for treatment of hypertension in 1979. Off-label low-dose oral minoxidil (≤5-mg/day) has been studied for androgenetic alopecia treatment,<ref>Randolph, M., & Tosti, A. (2021). Oral minoxidil treatment for hair loss: A review of efficacy and safety. Journal of the American Academy of Dermatology, 84(3), 737-746 PMID: 32622136 DOI: 10.1016/j.jaad.2020.06.1009</ref> and

	=== Application for stimulation of elastin expression ===		== Application for stimulation of elastin expression ==

	'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Rønnow, S. R., Kristensen, J. H., Thorlacius-Ussing, J., Karsdal, M. A., & Heinz, A. (2024). Elastin. In Biochemistry of Collagens, Laminins and Elastin (pp. 279-289). Academic Press. https://doi.org/10.1016/B978-0-443-15617-5.00016-0</ref><ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>		'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Rønnow, S. R., Kristensen, J. H., Thorlacius-Ussing, J., Karsdal, M. A., & Heinz, A. (2024). Elastin. In Biochemistry of Collagens, Laminins and Elastin (pp. 279-289). Academic Press. https://doi.org/10.1016/B978-0-443-15617-5.00016-0</ref><ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>
	Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />		Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />

	=== ~~Application~~ for ~~hair growth =~~==		== Treatment of pulmonary fibrosis ==
			Lysyl hydroxylase modify and crosslink proteins by converting lysine to hydroxylysine and so make collagen more resistant to degradation.<ref>Van Der Slot, A. J., Zuurmond, A. M., Van Den Bogaerdt, A. J., Ulrich, M. M., Middelkoop, E., Boers, W., ... & Bank, R. A. (2004). Increased formation of pyridinoline cross-links due to higher telopeptide lysyl hydroxylase levels is a general fibrotic phenomenon. Matrix biology, 23(4), 251-257.</ref> Minoxidil was reported to reduce lysyl hydroxylase activity by decreasing the lysine hydroxylase mRNA level.<ref>Hautala, T., Heikkinen, J., Kivirikko, K. I., & Myllylä, R. (1992). Minoxidil specifically decreases the expression of lysine hydroxylase in cultured human skin fibroblasts. Biochemical Journal, 283(1), 51-54.</ref><ref>Zuurmond, A. M., van der Slot-Verhoeven, A. J., van Dura, E. A., De Groot, J., & Bank, R. A. (2005). Minoxidil exerts different inhibitory effects on gene expression of lysyl hydroxylase 1, 2, and 3: implications for collagen cross-linking and treatment of fibrosis. Matrix biology, 24(4), 261-270.</ref> and thus reducing the formation of hydroxyallysine cross-links.<ref name="hydroxylase" >Shao, S., Zhang, X., Duan, L., Fang, H., Rao, S., Liu, W., ... & Zhang, X. (2018). Lysyl hydroxylase inhibition by minoxidil blocks collagen deposition and prevents pulmonary fibrosis via TGF-β1/Smad3 signaling pathway. Medical science monitor: international medical journal of experimental and clinical research, 24, 8592.PMID: 30481795 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278642/ PMC6278642] DOI: 10.12659/MSM.910761</ref> Thus minoxidil exert anti-fibrotic properties. However, these reducing effects of minoxidil on the pulmonary fibrosis were at least partly mediated via inhibition of the matrix metalloproteinases and TGF-β1/Smad3 signaling.<ref name="hydroxylase" />

	=== References ===		== Application for hair growth ==
			After minoxidil was was approved and marketed for the treatment of hypertension, clinicians learned that the drug stimulated hair growth.<ref>Zappacosta, A. R. (1980). Reversal of baldness in patient receiving minoxidil for hypertension. The New England Journal of Medicine, 303(25), 1480-1481. PMID: 7432414 DOI: 10.1056/nejm198012183032516</ref><ref>Suchonwanit, P., Thammarucha, S., & Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug design, development and therapy, 2777-2786. PMID: 31496654 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/ PMC6691938] DOI: 10.2147/DDDT.S214907</ref>
			<ref>Song, D., Pan, S., Jin, W., Wu, R., Zhao, T., Jiang, J., & Zhu, M. (2023). Minoxidil delivered via a stem cell membrane delivery controlled release system promotes hair growth in C57BL/6J mice. Frontiers in Bioengineering and Biotechnology, 11. PMID: 38260729 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10800965/ PMC10800965] DOI: 10.3389/fbioe.2023.1331754</ref> The mechanism of action of minoxidil on hair growth is probably not related to its effect on blood pressure in the vessels, since increased hair growth is observed even with very low doses of the drug (<5-mg/day) that do not cause a noticeable decrease in blood pressure.<ref>Ong, M., Do, H., Ho, B., & Lipner, S. R. (2024). Low-dose oral minoxidil for androgenetic alopecia is not associated with clinically significant blood-pressure changes: A retrospective study. Journal of the American Academy of Dermatology, 90(2), 425-427. PMID: 37839733 [https://doi.org/10.1016/j.jaad.2023.10.010 DOI: 10.1016/j.jaad.2023.10.010]</ref> Moreover, oral administration of the drug, even in such small doses, turned out to be a more effective way to stimulate hair growth than applying it to the skin.

			== References ==
	<references />		<references />
	[[Category:Drugs]]
			[[Category:Drugs]]
	[[Category:Drafts]]		[[Category:Drafts]]
	[[Category:~~Stub~~]]		[[Category:Main list]]

Dmitry Dzhagarov at 07:34, 6 February 2024

2024-02-06T07:34:59Z

← Older revision		Revision as of 07:34, 6 February 2024
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	'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906. </ref>		'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906.</ref>

	=== Application for stimulation of elastin expression ===		=== Application for stimulation of elastin expression ===

	'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Rønnow, S. R., Kristensen, J. H., Thorlacius-Ussing, J., Karsdal, M. A., & Heinz, A. (2024). Elastin. In Biochemistry of Collagens, Laminins and Elastin (pp. 279-289). Academic Press. https://doi.org/10.1016/B978-0-443-15617-5.00016-0</ref><ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>		'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Rønnow, S. R., Kristensen, J. H., Thorlacius-Ussing, J., Karsdal, M. A., & Heinz, A. (2024). Elastin. In Biochemistry of Collagens, Laminins and Elastin (pp. 279-289). Academic Press. https://doi.org/10.1016/B978-0-443-15617-5.00016-0</ref><ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>

Dmitry Dzhagarov: /* Application for stimulation of elastin expression */

2024-02-04T16:29:25Z

Application for stimulation of elastin expression

← Older revision		Revision as of 16:29, 4 February 2024
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	=== Application for stimulation of elastin expression ===		=== Application for stimulation of elastin expression ===

	'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>		'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Rønnow, S. R., Kristensen, J. H., Thorlacius-Ussing, J., Karsdal, M. A., & Heinz, A. (2024). Elastin. In Biochemistry of Collagens, Laminins and Elastin (pp. 279-289). Academic Press. https://doi.org/10.1016/B978-0-443-15617-5.00016-0</ref><ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>
	Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />		Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />

Dmitry Dzhagarov: /* References */

2024-02-04T10:32:36Z

References

← Older revision		Revision as of 10:32, 4 February 2024
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	<references />		<references />
	[[Category:Drugs]]		[[Category:Drugs]]
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	[[Category:Stub]]		[[Category:Stub]]

Dmitry Dzhagarov: /* Application for stimulation of elastin expression */

2024-02-03T20:34:17Z

Application for stimulation of elastin expression

← Older revision		Revision as of 20:34, 3 February 2024
Line 1:		Line 1:
	'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906. </ref>		'''Minoxidil''' is a potassium channel opener vasodilator.<ref>Nawar, T., Nolin, L., Plante, G. E., Caron, C., & Montambault, P. (1977). Long-term treatment of severe hypertension with minoxidil. Canadian Medical Association Journal, 117(10), 1178. PMID: 603847 PMC1880293</ref><ref>Campese, V. M. (1981). Minoxidil: a review of its pharmacological properties and therapeutic use. Drugs, 22, 257-278. https://doi.org/10.2165/00003495-198122040-00001</ref><ref>Gupta, A. K., Talukder, M., Venkataraman, M., & Bamimore, M. A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment, 33(4), 1896-1906. </ref>

	=== Application for stimulation of elastin expression ===		=== Application for stimulation of elastin expression ===

	'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref>		'''Elastin''' is a long-lived fibrous protein that is abundant in the extracellular matrix where it plays an important role in tissue elasticity.<ref>Trębacz, H., & Barzycka, A. (2023). Mechanical Properties and Functions of Elastin: An Overview. Biomolecules, 13(3), 574. PMID: 36979509 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046833/ PMC10046833] DOI: 10.3390/biom13030574</ref> In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality.<ref>Wang, K., Meng, X., & Guo, Z. (2021). Elastin structure, synthesis, regulatory mechanism and relationship with cardiovascular diseases. Frontiers in Cell and Developmental Biology, 9, 596702. PMID: 34917605 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8670233/ PMC8670233] DOI: 10.3389/fcell.2021.596702</ref><ref>Heinz, A. (2021). Elastic fibers during aging and disease. Ageing research reviews, 66, 101255. PMID: 33434682 [https://doi.org/10.1016/j.arr.2021.101255 DOI: 10.1016/j.arr.2021.101255]</ref> Elastin gene expression is limited to late embryonic and early postnatal development, so elastin cannot be replaced in aging arteries. At the same time elastin degrades with aging (elastin has a half-life of ∼70 yr), leading to a decrease in the elastin to collagen ratio and increased arterial stiffness.<ref>Cocciolone, A. J., Hawes, J. Z., Staiculescu, M. C., Johnson, E. O., Murshed, M., & Wagenseil, J. E. (2018). Elastin, arterial mechanics, and cardiovascular disease. American Journal of Physiology-Heart and Circulatory Physiology, 315(2), H189-H205. https://doi.org/10.1152/ajpheart.00087.2018</ref>
	Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />		Minoxidil can potentially stimulate elastogenesis in aortic smooth muscle cells,<ref>Coquand-Gandit, M., Jacob, M. P., Fhayli, W., Romero, B., Georgieva, M., Bouillot, S., ... & Faury, G. (2017). Chronic treatment with minoxidil induces elastic fiber neosynthesis and functional improvement in the aorta of aged mice. Rejuvenation research, 20(3), 218-230. PMID: 28056723 DOI: 10.1089/rej.2016.1874</ref><ref>Fhayli, W., Boyer, M., Ghandour, Z., Jacob, M. P., Andrieu, J. P., Starcher, B. C., ... & Faury, G. (2019). Chronic administration of minoxidil protects elastic fibers and stimulates their neosynthesis with improvement of the aorta mechanics in mice. Cellular Signalling, 62, 109333. PMID: 31176018 DOI: 10.1016/j.cellsig.2019.05.018</ref><ref>Knutsen, R. H., Beeman, S. C., Broekelmann, T. J., Liu, D., Tsang, K. M., Kovacs, A., ... & Kozel, B. A. (2018). Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness. American Journal of Physiology-Heart and Circulatory Physiology, 315(1), H18-H32. PMID: 29498532 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087770/ PMC6087770] DOI: 10.1152/ajpheart.00683.2017</ref><ref>Hayashi, A., Suzuki, T., Wachi, H., Tajima, S., Nishikawa, T., Murad, S., & Pinnell, S. R. (1994). Minoxidil stimulates elastin expression in aortic smooth muscle cells. Archives of biochemistry and biophysics, 315(1), 137-141. PMID: 7979390 [https://doi.org/10.1006/abbi.1994.1482 DOI: 10.1006/abbi.1994.1482]</ref><ref>Tajima, S. (1996). Modulation of elastin expression and cell proliferation in vascular smooth muscle cells in vitro. The Keio journal of medicine, 45(1), 58-62. PMID: 8882470 [https://doi.org/10.2302/kjm.45.58 DOI: 10.2302/kjm.45.58]</ref> and in skin fibroblasts<ref>Tajima, S., Hayashi, A., Suzuki, T., & Nishikawa, T. (1995). Stimulation of elastin expression by minoxidil in chick skin fibroblasts. Archives of dermatological research, 287, 494-497. PMID: 7625861 [https://doi.org/10.1007/BF00373434 DOI: 10.1007/BF00373434]</ref> in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin level in the mesenteric, abdominal, and renal arteries by a decrease in "elastase" enzyme activity in these tissues.<ref>Tsoporis, J., Fields, N., Lee, R. M., & Leenen, F. H. (1993). Effects of the arterial vasodilator minoxidil on cardiovascular structure and sympathetic activity in spontaneously hypertensive rats. Journal of hypertension, 11(12), 1337-1345. PMID: 8133016 [https://doi.org/10.1097/00004872-199312000-00004 DOI: 10.1097/00004872-199312000-00004]</ref> In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase ½ (ERK 1/2)-activator protein 1 signaling pathway.<ref name="aorta" >Lannoy, M., Slove, S., Louedec, L., Choqueux, C., Journé, C., Michel, J. B., & Jacob, M. P. (2014). Inhibition of ERK1/2 phosphorylation: a new strategy to stimulate elastogenesis in the aorta. Hypertension, 64(2), 423-430. PMID: 24866134 [https://doi.org/10.1161/HYPERTENSIONAHA.114.03352 DOI: 10.1161/HYPERTENSIONAHA.114.03352]</ref><ref name="stenosis" >Lin, C. J., Cocciolone, A. J., & Wagenseil, J. E. (2022). Elastin, arterial mechanics, and stenosis. American Journal of Physiology-Cell Physiology, 322(5), C875-C886. PMID: 35196168 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9037699/ PMC9037699] DOI: 10.1152/ajpcell.00448.2021</ref> ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.<ref name="aorta" /><ref name="stenosis" />