Seno-protective benefits of tropoelastin

Accelerated elastin degradation by age-disease interaction: a common feature in age-related diseases.

 "... Ultra-long lived proteins such as elastin, collagen, and eye lens crystalline have been considered as the Achilles heel of the aging proteome as their damages and losses are not easily repaired. Among them, elastin is unique in providing the characteristics of elasticity, resilience, and deformability of tissues such as the aorta, lung, and skin etc, and its fragmentation and degradation represents an important feature of normal aging. Elastin is a crosslinked polymeric network of tropoelastin monomers catalysed by lysine oxidase during development. In adult tissues, elastin has an extremely low turnover rate with a half-life of ~74 years under normal conditions in contrast to minutes to days for most intracellular proteins. In general, adult tissues lack the capability of regenerating functional elastic fibre. These two unique properties imply that an increased turnover of this ultra-long-lived protein in adult tissues could result in irreversible changes to elastin-rich tissues. ..."

Despite the above mentioned, evidence has emerged that to some extent this elastin network is still being renewed. Moreover, in vitro experiments have even demonstrated that the addition of endogenous tropoelastin (the soluble monomer of elastin) prolongs mesenchymal stromal/stem cells (MSCs) vitality and delays senescence during replicative aging.