Abstract：
:Mammalian models of longevity are related primarily to caloric restriction and alterations in metabolism. We examined mice in which type 5 adenylyl cyclase (AC5) is knocked out (AC5 KO) and which are resistant to cardiac stress and have increased median lifespan of approximately 30%. AC5 KO mice are protected from reduced bone density and susceptibility to fractures of aging. Old AC5 KO mice are also protected from aging-induced cardiomyopathy, e.g., hypertrophy, apoptosis, fibrosis, and reduced cardiac function. Using a proteomic-based approach, we demonstrate a significant activation of the Raf/MEK/ERK signaling pathway and upregulation of cell protective molecules, including superoxide dismutase. Fibroblasts isolated from AC5 KO mice exhibited ERK-dependent resistance to oxidative stress. These results suggest that AC is a fundamentally important mechanism regulating lifespan and stress resistance.
journal_name
Celljournal_title
Cellauthors
Yan L,Vatner DE,O'Connor JP,Ivessa A,Ge H,Chen W,Hirotani S,Ishikawa Y,Sadoshima J,Vatner SFdoi
10.1016/j.cell.2007.05.038subject
Has Abstractpub_date
2007-07-27 00:00:00pages
247-58issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(07)00677-0journal_volume
130pub_type
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