Journal
SCIENCE
Volume 309, Issue 5742, Pages 1829-1833Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1112766
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Funding
- NHLBI NIH HHS [R37 HL063762] Funding Source: Medline
- NIA NIH HHS [R01 AG019712-05, R01 AG025326, R01 AG025326-03, R01 AG019712, R01AG25326, R01AG19712] Funding Source: Medline
- NIDDK NIH HHS [U24 DK059637] Funding Source: Medline
- Div Of Information & Intelligent Systems
- Direct For Computer & Info Scie & Enginr [0829438] Funding Source: National Science Foundation
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A defect in Klotho gene expression in mice accelerates the degeneration of multiple age-sensitive traits. Here, we show that overexpression of Klotho in mice extends life span. Klotho protein functions as a circulating hormone that binds to a cell-surface receptor and represses intracellular signals of insulin and insulin-like growth factor 1 (IGF1), an evolutionarily conserved mechanism for extending life span. Alleviation of aging-like phenotypes in Klotho-deficient mice was observed by perturbing insulin and IGF1 signaling, suggesting that Klotho-mediated inhibition of insulin and IGF1 signaling contributes to its anti-aging properties. Klotho protein may function as an anti-aging hormone in mammals.
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