Many research groups around the world are all gnawing away at their own little pieces of the very large and complex web of interactions between proteins in particular areas of age-related degeneration. Here is work focused on a narrow portion of the biochemistry of progressive loss of muscle mass and function:
The loss of muscle mass in older subjects, termed sarcopenia, not only decreases muscle strength, contributing to a high incidence of accidental falls and injuries but also compromising the quality of life of elderly subjects. Identification of mechanisms and contributors to aging-induced muscle loss could lead to new therapeutic strategies for preventing and treating sarcopenia. Thus, we examined mechanisms causing sarcopenia and the development of muscle cell senescence in both mice and rats, [and] found that the microRNA miR-29 can initiate muscle cell senescence leading to aging-induced sarcopenia. miR-29 was increased in muscles of both mice and rats and it was associated with the presence of higher levels of cellular arrest proteins and lower levels of cell proliferation.
Expression of miR-29 suppressed the expression of IGF-1 and p85α and B-myb and led to induction of senescence in vivo. Thus, the presence of senescent cells that are derived from muscle progenitor cells (MPCs) would contribute to an exhaustion of MPCs regeneration, contributing to the development of muscle atrophy and sarcopenia. In vivo, electroporation of miR-29 into muscles of young mice suppressed the proliferation and increased levels of cellular arrest proteins, recapitulating aging-induced responses in muscle. A potential stimulus of miR-29 expression is Wnt-3a since we found that exogenous Wnt-3a stimulated mir-29 expression 2.7-fold in primary cultures of MPCs. The increase in miR-29 provides a potential mechanism for aging-induced sarcopenia.