Researchers here report on another way to tell old stem cells to get back to work on maintaining muscle tissue - though not one that has immediate application, as it requires removal of an important component of immune system function. Thus this is only promising if researchers can pick apart the different functions of this component and interfere only where it suppresses stem cell activity in muscle regeneration: "Wnt signaling plays critical roles in development of various organs and pathogenesis of many diseases, and augmented Wnt signaling has recently been implicated in mammalian aging and aging-related phenotypes. We here report that complement C1q activates canonical Wnt signaling and promotes aging-associated decline in tissue regeneration. Serum C1q concentration is increased with aging, and Wnt signaling activity is augmented during aging in the serum and in multiple tissues of wild-type mice, but not in those of C1qa-deficient mice. ... Skeletal muscle regeneration in young mice is inhibited by exogenous C1q treatment, whereas aging-associated impairment of muscle regeneration is restored by C1s inhibition or C1qa gene disruption. Our findings therefore suggest the unexpected role of complement C1q in Wnt signal transduction and modulation of mammalian aging."

Link: http://www.cell.com/retrieve/pii/S0092867412005314

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm