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. 2007 Jul 27;130(2):247-58.
doi: 10.1016/j.cell.2007.05.038.

Type 5 adenylyl cyclase disruption increases longevity and protects against stress

Lin Yan  1 , Dorothy E Vatner, J Patrick O'Connor, Andreas Ivessa, Hui Ge, Wei Chen, Shinichi Hirotani, Yoshihiro Ishikawa, Junichi Sadoshima, Stephen F Vatner
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Free article

Type 5 adenylyl cyclase disruption increases longevity and protects against stress

Lin Yan et al. Cell. .
Free article

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.

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