Cellular senescence - Revision history

Dmitry Dzhagarov: /* SASP */

2024-07-21T17:52:53Z

SASP

← Older revision		Revision as of 17:52, 21 July 2024
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	\| Chemokines \|\| IL-8, GROα, GROβ, GROγ, MCP1, MCP2, MCP4, CCL1, CCL3, CCL5, CCL11, CCL16, CCL20, CCL25, CCL26		\| Chemokines \|\| IL-8, GROα, GROβ, GROγ, MCP1, MCP2, MCP4, CCL1, CCL3, CCL5, CCL11, CCL16, CCL20, CCL25, CCL26
	\|-		\|-
	\| Cytokines \|\| IL-6, IL-7, IL-1α, IL-1b, IL-13, IL-15, IL23a, TNFα		\| Cytokines \|\| IL-6, [[Interleukin-11 (IL-11)\|'''IL-11''']]*, IL-7, IL-1α, IL-1b, IL-13, IL-15, IL23a, TNFα
	\|-		\|-
	\| Other inflammatory factors \|\| TGF-β, GM-CSF, M-CSF, G-CSF, IFN-α1, IFN-γ, CCL13, MIF, LIF		\| Other inflammatory factors \|\| TGF-β, GM-CSF, M-CSF, G-CSF, IFN-α1, IFN-γ, CCL13, MIF, LIF
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	\|-		\|-
	\| Insoluble molecules \|\| Collagens, fibronectin, laminin		\| Insoluble molecules \|\| Collagens, fibronectin, laminin
			\|-
			\|+ *Added by us later based on literature data
	\|-		\|-
	\|}		\|}

	Data are derived and processed from cellular senescence- and aging-related literatures (Acosta et al., 2008; Coppe et al., 2008a; Coppe et al., 2010; Coppe et al., 2008b; Gorgoulis et al., 2019; Kuilman et al., 2008; Rodier et al., 2011; Sun et al., 2012). See also: Wang et al., 2024<ref>Wang, B., Han, J., Elisseeff, J.H. et al. (2024). The senescence-associated secretory phenotype and its physiological and pathological implications. Nat Rev Mol Cell Biol https://doi.org/10.1038/s41580-024-00727-x </ref>		Data are derived and processed from cellular senescence- and aging-related literatures (Acosta et al., 2008; Coppe et al., 2008a; Coppe et al., 2010; Coppe et al., 2008b; Gorgoulis et al., 2019; Kuilman et al., 2008; Rodier et al., 2011; Sun et al., 2012). See also: Wang et al., 2024<ref>Wang, B., Han, J., Elisseeff, J.H. et al. (2024). The senescence-associated secretory phenotype and its physiological and pathological implications. Nat Rev Mol Cell Biol https://doi.org/10.1038/s41580-024-00727-x </ref>

Dmitry Dzhagarov: /* Senolytics */

2024-06-21T19:37:03Z

Senolytics

← Older revision		Revision as of 19:37, 21 June 2024
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	A way to track if senolytics have any effect is to check out for ''senescent biomarkers''. Some known markers of SCs are p16, p21 and senescence-associated β-galactosidase activity (SA-β-gal).		A way to track if senolytics have any effect is to check out for ''senescent biomarkers''. Some known markers of SCs are p16, p21 and senescence-associated β-galactosidase activity (SA-β-gal).

	https://brain.forever-healthy.org/display/EN/Dasatinib+and+Quercetin+Senolytic+Therapy		https://brain.forever-healthy.org/display/EN/Dasatinib+and+Quercetin+Senolytic+Therapy

			=== Cellular senescence as an adaptive process ===
			* <ref>João Pedro de Magalhães (2024). [https://www.science.org/doi/10.1126/science.adj7050 Cellular senescence in normal physiology].Science, 384, 1300-1301 DOI:10.1126/science.adj7050</ref>

	=== Negligible senescence ===		=== Negligible senescence ===

Dmitry Dzhagarov: /* Mechanism */

2024-06-20T11:18:19Z

Mechanism

← Older revision		Revision as of 11:18, 20 June 2024
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	=== Mechanism ===		=== Mechanism ===

	Senescent cells produce pro-inflammatory signalling molecules such as the ''senescence-associated secretory phenotype'' (SASP), releasing various factors that can trigger inflammation and dysfunction, while promoting apoptosis (cell death) in nearby tissues.		Senescent cells produce pro-inflammatory signalling molecules such as the ''senescence-associated secretory phenotype'' (SASP),<ref>Huna, A., Massemin, A., Makulyte, G., Flaman, J. M., Martin, N., & Bernard, D. (2024). Regulation of cell function and identity by cellular senescence. Journal of Cell Biology, 223(8). PMID: 38865089 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11169915/ PMC11169915] DOI: 10.1083/jcb.202401112</ref> releasing various factors that can trigger inflammation and dysfunction, while promoting apoptosis (cell death) in nearby tissues.

	==== SASP ====		==== SASP ====

Dmitry Dzhagarov: /* SASP */

2024-04-25T09:39:03Z

SASP

← Older revision		Revision as of 09:39, 25 April 2024
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	\|-		\|-
	\|}		\|}
	Data are derived and processed from cellular senescence- and aging-related literatures (Acosta et al., 2008; Coppe et al., 2008a; Coppe et al., 2010; Coppe et al., 2008b; Gorgoulis et al., 2019; Kuilman et al., 2008; Rodier et al., 2011; Sun et al., 2012).		Data are derived and processed from cellular senescence- and aging-related literatures (Acosta et al., 2008; Coppe et al., 2008a; Coppe et al., 2010; Coppe et al., 2008b; Gorgoulis et al., 2019; Kuilman et al., 2008; Rodier et al., 2011; Sun et al., 2012). See also: Wang et al., 2024<ref>Wang, B., Han, J., Elisseeff, J.H. et al. (2024). The senescence-associated secretory phenotype and its physiological and pathological implications. Nat Rev Mol Cell Biol https://doi.org/10.1038/s41580-024-00727-x </ref>

	Circulating concentrations of senescence biomarkers of the SASP, could predict mortality in older adults. Elevated levels of a stress-induced cytokine growth factor '''GDF15 are most strongly associated with an increased risk of death''' in populations of all ages, even after adjustment for several risk factors.<ref>Eggers, K. M., Kempf, T., Wallentin, L., Wollert, K. C., & Lind, L. (2013). Change in growth differentiation factor 15 concentrations over time independently predicts mortality in community-dwelling elderly individuals. Clinical Chemistry, 59(7), 1091–1098. https://doi.org/10.1373/clinchem.2012.201210</ref><ref>St. Sauver, J. L., Weston, S. A., Atkinson, E. J., Mc Gree, M. E., Mielke, M. M., White, T. A., ... & LeBrasseur, N. K. (2023). Biomarkers of cellular senescence and risk of death in humans. Aging Cell, e14006. https://doi.org/10.1111/acel.14006</ref><ref>Wischhusen, J., Melero, I., & Fridman, W. H. (2020). Growth/differentiation Factor-15 (GDF-15): From biomarker to novel targetable immune checkpoint. Frontiers in Immunology, 11, 951. https://doi.org/10.3389/fimmu.2020.00951</ref><ref>Wan, Y., & Fu, J. (2023). GDF15 as a key disease target and biomarker: linking chronic lung diseases and ageing. Molecular and Cellular Biochemistry, 1-14. PMID: 37093513 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10123484/ PMC10123484] DOI: 10.1007/s11010-023-04743-x</ref>		Preliminary identification of specific SASP proteins associated with aging traits in humans was carried out in the work of Evans et al., 2024. <ref name="Evans" >Evans, D. S., Young, D., Tanaka, T., Basisty, N., Bandinelli, S., Ferrucci, L., ... & Schilling, B. Proteomic Analysis of the Senescence Associated Secretory Phenotype (SASP): GDF-15, IGFBP-2, and Cystatin-C Are Associated with Multiple Aging Traits. The journals of gerontology. Series A, Biological sciences and medical sciences, 79(3), glad265. PMID: 37982669 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10876076/ PMC10876076] DOI: 10.1093/gerona/glad265</ref> Among the 28 age-associated SASP proteins, 18 were associated with 1 or more clinical age-related traits. '''GDF-15''' (Growth/differentiation factor 15), CST3 (Cystatin 3) also known as '''Cystatin-C''' (lysosomal and extracellular cysteine protease inhibitor С), and '''IGFBP-2''' (Insulin-like growth factor-binding protein 2) were the most significantly associated with age, and each of these proteins was associated with 5 or more clinical traits. GDF-15 and IGFBP-2 were both significantly associated with age, inflammatory markers, fasting glucose, RDW, albumin, and grip strength. Higher levels of Cystatin-C were significantly associated with higher IL6, higher BUN, lower albumin, and poorer physical performance (lower grip strength and slower gait speed), and higher levels of Cystatin-C’s target, Cathepsin Z, were significantly associated with higher waist circumference, higher CRP, and slower gait speed.<ref name="Evans" />

			Circulating concentrations of senescence biomarkers of the SASP, could predict mortality in older adults. Elevated levels of a stress-induced cytokine growth factor '''GDF15 are most strongly associated with an increased risk of death''' in populations of all ages, even after adjustment for several risk factors.<ref>Eggers, K. M., Kempf, T., Wallentin, L., Wollert, K. C., & Lind, L. (2013). Change in growth differentiation factor 15 concentrations over time independently predicts mortality in community-dwelling elderly individuals. Clinical Chemistry, 59(7), 1091–1098. https://doi.org/10.1373/clinchem.2012.201210</ref><ref>St. Sauver, J. L., Weston, S. A., Atkinson, E. J., Mc Gree, M. E., Mielke, M. M., White, T. A., ... & LeBrasseur, N. K. (2023). Biomarkers of cellular senescence and risk of death in humans. Aging Cell, e14006. https://doi.org/10.1111/acel.14006</ref><ref>Wischhusen, J., Melero, I., & Fridman, W. H. (2020). Growth/differentiation Factor-15 (GDF-15): From biomarker to novel targetable immune checkpoint. Frontiers in Immunology, 11, 951. https://doi.org/10.3389/fimmu.2020.00951</ref><ref>Wan, Y., & Fu, J. (2023). GDF15 as a key disease target and biomarker: linking chronic lung diseases and ageing. Molecular and Cellular Biochemistry, 1-14. PMID: 37093513 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10123484/ PMC10123484] DOI: 10.1007/s11010-023-04743-x</ref><ref name="Evans" />

	=== Cellular senescence and aging ===		=== Cellular senescence and aging ===

Dmitry Dzhagarov at 16:00, 10 December 2023

2023-12-10T16:00:14Z

← Older revision		Revision as of 16:00, 10 December 2023
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	~~{{Draft-article}}~~

	Senescent cells (SCs) are cells that have stopped dividing and are no longer able to grow or divide, a phenomenon known as the "Hayflick limit".<ref>Shay, J., Wright, W. Hayflick, his limit, and cellular ageing. ''Nat Rev Mol Cell Biol'' 1, 72–76 (2000). <nowiki>https://doi.org/10.1038/35036093</nowiki></ref> SCs have been hypothesized to be drivers of aging and are associated to aging and age-related diseaeses.<ref name=":0">van Deursen JM. The role of senescent cells in ageing. Nature. 2014 May 22;509(7501):439-46. doi: 10.1038/nature13193. PMID: 24848057; PMCID: PMC4214092.</ref> Cellular senescence is considered to be one of the [[Hallmarks of Aging\|hallmarks of aging]].<ref>López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. ''Cell'', ''153''(6), 1194-1217.</ref>		Senescent cells (SCs) are cells that have stopped dividing and are no longer able to grow or divide, a phenomenon known as the "Hayflick limit".<ref>Shay, J., Wright, W. Hayflick, his limit, and cellular ageing. ''Nat Rev Mol Cell Biol'' 1, 72–76 (2000). <nowiki>https://doi.org/10.1038/35036093</nowiki></ref> SCs have been hypothesized to be drivers of aging and are associated to aging and age-related diseaeses.<ref name=":0">van Deursen JM. The role of senescent cells in ageing. Nature. 2014 May 22;509(7501):439-46. doi: 10.1038/nature13193. PMID: 24848057; PMCID: PMC4214092.</ref> Cellular senescence is considered to be one of the [[Hallmarks of Aging\|hallmarks of aging]].<ref>López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. ''Cell'', ''153''(6), 1194-1217.</ref>

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	The phenomenon of showing no signs of senescence, such as age-related dysfunctions.		The phenomenon of showing no signs of senescence, such as age-related dysfunctions.

			== References ==
			<references />
	[[Category:Main list]]		[[Category:Main list]]
	[[Category:Aging pathways and hallmarks]]		[[Category:Aging pathways and hallmarks]]
			[[Category:Drafts]]

Dmitry Dzhagarov: /* SASP */

2023-10-10T04:02:46Z

SASP

← Older revision		Revision as of 04:02, 10 October 2023
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	\|}		\|}
	Data are derived and processed from cellular senescence- and aging-related literatures (Acosta et al., 2008; Coppe et al., 2008a; Coppe et al., 2010; Coppe et al., 2008b; Gorgoulis et al., 2019; Kuilman et al., 2008; Rodier et al., 2011; Sun et al., 2012).		Data are derived and processed from cellular senescence- and aging-related literatures (Acosta et al., 2008; Coppe et al., 2008a; Coppe et al., 2010; Coppe et al., 2008b; Gorgoulis et al., 2019; Kuilman et al., 2008; Rodier et al., 2011; Sun et al., 2012).

			Circulating concentrations of senescence biomarkers of the SASP, could predict mortality in older adults. Elevated levels of a stress-induced cytokine growth factor '''GDF15 are most strongly associated with an increased risk of death''' in populations of all ages, even after adjustment for several risk factors.<ref>Eggers, K. M., Kempf, T., Wallentin, L., Wollert, K. C., & Lind, L. (2013). Change in growth differentiation factor 15 concentrations over time independently predicts mortality in community-dwelling elderly individuals. Clinical Chemistry, 59(7), 1091–1098. https://doi.org/10.1373/clinchem.2012.201210</ref><ref>St. Sauver, J. L., Weston, S. A., Atkinson, E. J., Mc Gree, M. E., Mielke, M. M., White, T. A., ... & LeBrasseur, N. K. (2023). Biomarkers of cellular senescence and risk of death in humans. Aging Cell, e14006. https://doi.org/10.1111/acel.14006</ref><ref>Wischhusen, J., Melero, I., & Fridman, W. H. (2020). Growth/differentiation Factor-15 (GDF-15): From biomarker to novel targetable immune checkpoint. Frontiers in Immunology, 11, 951. https://doi.org/10.3389/fimmu.2020.00951</ref><ref>Wan, Y., & Fu, J. (2023). GDF15 as a key disease target and biomarker: linking chronic lung diseases and ageing. Molecular and Cellular Biochemistry, 1-14. PMID: 37093513 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10123484/ PMC10123484] DOI: 10.1007/s11010-023-04743-x</ref>

	=== Cellular senescence and aging ===		=== Cellular senescence and aging ===

Dmitry Dzhagarov: /* Mechanism */

2023-05-03T14:36:45Z

Mechanism

← Older revision		Revision as of 14:36, 3 May 2023
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	Senescent cells produce pro-inflammatory signalling molecules such as the ''senescence-associated secretory phenotype'' (SASP), releasing various factors that can trigger inflammation and dysfunction, while promoting apoptosis (cell death) in nearby tissues.		Senescent cells produce pro-inflammatory signalling molecules such as the ''senescence-associated secretory phenotype'' (SASP), releasing various factors that can trigger inflammation and dysfunction, while promoting apoptosis (cell death) in nearby tissues.

			==== SASP ====
			'''Typical components and central biomarkers of the SASP according to Aging Biomarker Consortium., Bao, H., Cao, J. et al. 2023'''<ref>Aging Biomarker Consortium., Bao, H., Cao, J. et al. (2023). '''Biomarkers of aging'''. ''Sci. China Life Sci.'' https://doi.org/10.1007/s11427-023-2305-0</ref>
			{\| class="wikitable"
			\|-
			! Subcategory !! Component
			\|-
			\| Chemokines \|\| IL-8, GROα, GROβ, GROγ, MCP1, MCP2, MCP4, CCL1, CCL3, CCL5, CCL11, CCL16, CCL20, CCL25, CCL26
			\|-
			\| Cytokines \|\| IL-6, IL-7, IL-1α, IL-1b, IL-13, IL-15, IL23a, TNFα
			\|-
			\| Other inflammatory factors \|\| TGF-β, GM-CSF, M-CSF, G-CSF, IFN-α1, IFN-γ, CCL13, MIF, LIF
			\|-
			\| Growth factors \|\| AREG, EREG, heregulin, EGF, bFGF, HGF, FGF7, VEGF, ANG, SCF, CXCL12, GDF15, GDNF, IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP6, IGFBP7
			\|-
			\| Proteases and inhibitors \|\| MMP1, MMP2, MMP3, MMP8, MMP10, MMP12, MMP14, TIMP1, TIMP2, PAI-1, PAI-2, tPA, uPA, cathepsin B, SPINK1, SERPINs
			\|-
			\| Receptors and ligands \|\| ICAM1, ICAM3, OPG, sTNFRI, sTNFRII, TRAIL-R3, Fas, uPAR, SGP130, EGF-R, WNT16B
			\|-
			\| Insoluble molecules \|\| Collagens, fibronectin, laminin
			\|-
			\|}
			Data are derived and processed from cellular senescence- and aging-related literatures (Acosta et al., 2008; Coppe et al., 2008a; Coppe et al., 2010; Coppe et al., 2008b; Gorgoulis et al., 2019; Kuilman et al., 2008; Rodier et al., 2011; Sun et al., 2012).

	=== Cellular senescence and aging ===		=== Cellular senescence and aging ===

Andrea: Updated entry

2023-02-01T18:10:03Z

Updated entry

← Older revision		Revision as of 18:10, 1 February 2023
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	{{Draft-article}}		{{Draft-article}}

	Cellular senescence is one of the [[Hallmarks of Aging\|hallmarks of aging]].		Senescent cells (SCs) are cells that have stopped dividing and are no longer able to grow or divide, a phenomenon known as the "Hayflick limit".<ref>Shay, J., Wright, W. Hayflick, his limit, and cellular ageing. ''Nat Rev Mol Cell Biol'' 1, 72–76 (2000). <nowiki>https://doi.org/10.1038/35036093</nowiki></ref> SCs have been hypothesized to be drivers of aging and are associated to aging and age-related diseaeses.<ref name=":0">van Deursen JM. The role of senescent cells in ageing. Nature. 2014 May 22;509(7501):439-46. doi: 10.1038/nature13193. PMID: 24848057; PMCID: PMC4214092.</ref> Cellular senescence is considered to be one of the [[Hallmarks of Aging\|hallmarks of aging]].<ref>López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. ''Cell'', ''153''(6), 1194-1217.</ref>

	== Mechanism ==		=== Mechanism ===
	''Question to writers: Cellular senescence seems to have a positive function in our bodies - what is that? How does it become dangerous? It seems like it is "a normally adaptive response to injury or infection". Source: <nowiki>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941545/</nowiki>''

	Senescent cells ~~secrete a phenotype, appropriately called~~ ''senescence-associated secretory phenotype'' (SASP), ~~which releases~~ various factors that ~~cause~~ inflammation and dysfunction ~~and promotes~~ apoptosis (cell death) in nearby tissues.		Senescent cells produce pro-inflammatory signalling molecules such as the ''senescence-associated secretory phenotype'' (SASP), releasing various factors that can trigger inflammation and dysfunction, while promoting apoptosis (cell death) in nearby tissues.

			=== Cellular senescence and aging ===
			Due to the negative impact that SCs may have in neighbouring cells and tissues, some scientists believe that the clearance of senescent cells via [[senolytics]] may have therapeutic benefits, especially for treating age-related diseases such as cancer, cardiovascular disease or neurodegeneration.<ref name=":0" /> Cellular senescence has also been suggested as a driver of fibrotic pulmonary disease.<ref>Schafer MJ, White TA, Iijima K, Haak AJ, Ligresti G, Atkinson EJ, Oberg AL, Birch J, Salmonowicz H, Zhu Y, Mazula DL, Brooks RW, Fuhrmann-Stroissnigg H, Pirtskhalava T, Prakash YS, Tchkonia T, Robbins PD, Aubry MC, Passos JF, Kirkland JL, Tschumperlin DJ, Kita H, LeBrasseur NK. Cellular senescence mediates fibrotic pulmonary disease. Nat Commun. 2017 Feb 23;8:14532. doi: 10.1038/ncomms14532. PMID: 28230051; PMCID: PMC5331226.</ref>

	''~~Source references are needed for all of~~ the ~~above~~, ~~for example:~~''		Cellular senescence can be viewed as a necessary, adaptive response of the body in response to injury, infection or other stresses.<ref>Tchkonia T, Morbeck DE, Von Zglinicki T, Van Deursen J, Lustgarten J, Scrable H, Khosla S, Jensen MD, Kirkland JL. Fat tissue, aging, and cellular senescence. Aging Cell. 2010 Oct;9(5):667-84. doi: 10.1111/j.1474-9726.2010.00608.x. Epub 2010 Aug 15. PMID: 20701600; PMCID: PMC2941545.</ref> It also serves key purposes during tissue remodelling, wound repair or embryogenesis. However, chronic senescence can be maladaptive and lead to age-related diseases.<ref>Huang, W., Hickson, L.J., Eirin, A. ''et al.'' Cellular senescence: the good, the bad and the unknown. ''Nat Rev Nephrol'' 18, 611–627 (2022). <nowiki>https://doi.org/10.1038/s41581-022-00601-z</nowiki></ref>

	https://~~brain~~.~~forever-healthy~~.~~org~~/~~display~~/EN/~~Dasatinib+and+Quercetin+Senolytic+Therapy~~		It is not clear whether removing senescent cells might have deleterious effects ''in vivo,'' and several studies are suggesting that they play a fundamental role in physiology and thus might be detrimental to remove them, even when accumulated chronically. For instance, eliminating senescent cells in mice promoted the development and progression of pulmonary hypertension.<ref>Born, E. ''et al.'' (2022) “Eliminating senescent cells can promote pulmonary hypertension development and progression,” ''Circulation''[Preprint]. Available at: <nowiki>https://doi.org/10.1161/circulationaha.122.058794</nowiki>.</ref>

	=== ~~Diseases associated with cellular senescence ===~~		=== Senolytics ===
	~~Due to the SASP, senescent cells have been associated with a number of age-related diseases:~~

	~~<nowiki>*</nowiki>Fibrotic Pulmonary Disease: <nowiki>https://pubmed.ncbi.nlm.nih.gov/28230051/</nowiki>~~

	=~~= Senolytics~~ ==
	''See the full article on [[senolytics]].''		''See the full article on [[senolytics]].''

	Senescent cells survive their own SASP, since they are protected by networks of ''senescent cell anti-apoptotic pathways'' (SCAPs). One ~~method~~ of senolytics, therefore, is to interfere with these networks, so that the SASP also induce apoptosis in the senescent cells themselves.		Senescent cells survive their own SASP, since they are protected by networks of ''senescent cell anti-apoptotic pathways'' (SCAPs). One mechanism of senolytics, therefore, is to interfere with these networks, so that the SASP also induce apoptosis in the senescent cells themselves. Senescent cells take time to re-build once they are ablated. Hence, an advantage of senolytic treatment is that it can be done in a "hit-and-run" fashion, thus avoiding off-target effects in comparison to other types of treatments.

	Senescent cells take time to re-build once they are ablated. Hence, an advantage of senolytic treatment is that it can be done in a "hit-and-run" fashion, thus avoiding off-target effects in comparison to other types of treatments.

	A way to track if senolytics have any effect is to check out for ''senescent biomarkers''. It seems like p16, p21 and senescence-associated β-galactosidase activity (SA-β-gal) are known markers of senescent cells.

	''~~Writers: Make sure to sync this article with senolytics.~~''		A way to track if senolytics have any effect is to check out for ''senescent biomarkers''. Some known markers of SCs are p16, p21 and senescence-associated β-galactosidase activity (SA-β-gal).

	~~''Source references are needed for all of the above, see for example the three human clinical trial studies in the article on [[dasatinib]]~~.''		https://brain.forever-healthy.org/display/EN/Dasatinib+and+Quercetin+Senolytic+Therapy

	== Negligible senescence ==		=== Negligible senescence ===
	''See the full article on [[negligible senescence]].''		''See the full article on [[negligible senescence]].''

	The phenomenon of showing no signs of senescence, such as age-related dysfunctions ~~(Wikipedia)~~.		The phenomenon of showing no signs of senescence, such as age-related dysfunctions.
	[[Category:Main list]]		[[Category:Main list]]
	[[Category:Aging pathways and hallmarks]]		[[Category:Aging pathways and hallmarks]]

Andrea: category change

2022-12-27T12:48:27Z

category change

← Older revision		Revision as of 12:48, 27 December 2022
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	The phenomenon of showing no signs of senescence, such as age-related dysfunctions (Wikipedia).		The phenomenon of showing no signs of senescence, such as age-related dysfunctions (Wikipedia).
	[[Category:Main list]]		[[Category:Main list]]
	[[Category:~~Hallmarks of aging~~]]		[[Category:Aging pathways and hallmarks]]

Andrea: category change

2022-12-27T12:00:47Z

category change

← Older revision		Revision as of 12:00, 27 December 2022
Line 35:		Line 35:

	The phenomenon of showing no signs of senescence, such as age-related dysfunctions (Wikipedia).		The phenomenon of showing no signs of senescence, such as age-related dysfunctions (Wikipedia).
	[[Category:~~Longevity~~]]		[[Category:Main list]]
			[[Category:Hallmarks of aging]]