Journal
GERONTOLOGY
Volume 60, Issue 1, Pages 56-64Publisher
KARGER
DOI: 10.1159/000354382
Keywords
Sirtuin; Mitochondria; Deacetylase; Acetylation; Metabolism; Reactive oxygen species; Adenosine monophosphate-activated protein kinase; PGC1 alpha
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Funding
- NIH [R01GM101171, R21CA177925]
- Ellison Medical Foundation [AG-NS-0583-09]
- Discovery Fund of the University of Michigan Comprehensive Cancer Center
- NATIONAL CANCER INSTITUTE [R21CA177925] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK020572] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM101171] Funding Source: NIH RePORTER
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Identification of conserved pathways regulating longevity holds out the eventual possibility of pharmacologic health- and lifespan extension in humans. Members of the sirtuin deacetylase/ADP-ribosyltransferase/deacylase family extend longevity in invertebrates and promote various aspects of mammalian healthspan. The mitochondria! sirtuin SIRT3 deacetylates numerous proteins in this organelle, regulating mitochondrial functions and suppressing diverse age-associated pathologies. However, recent findings raise the possibility that SIRT3 may regulate some mitochondrial functions indirectly, rather than by direct deacetylation of specific mitochondrial substrates. Specifically, it has been found that SIRT3 promotes activities of the upstream mitochondrial regulators adenosine monophosphate-activated protein kinase and PGC1 alpha. In addition, studies of tissue-specific SIRT3 knockouts suggest non-tissue-autonomous roles for SIRT3. Thus, mitochondrial regulation by SIRT3 is likely much more complex than initially appreciated, potentially involving both direct and indirect mechanisms. Unraveling these may reveal novel aspects of how the functional status of the mitochondria is communicated to the rest of the cell, and to the organism overall. (C) 2013 S. Karger AG, Basel
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