Journal
DNA REPAIR
Volume 23, Issue -, Pages 64-68Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2014.08.005
Keywords
Heart; Ischemia; Reperfusion; NAD; Sirt1; Apoptosis
Categories
Funding
- U.S. Public Health Service [HL102738, HL67724, HL69020, HL91469, AG23039, AG27211]
- Fondation Leducq Transatlantic Networks of Excellence
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL112330, R01HL091469, R01HL102738, R01HL067724, P01HL069020] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG027211, R01AG023039] Funding Source: NIH RePORTER
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In addition to its roles as a coenzyme and an electron transfer molecule, nicotinamide adenine dinucleotide (NAD+) has emerged as a substrate of sirtuins, a family of enzymes that control aging and metabolism. Nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme in the NAD+ salvage pathway, plays an important role in controlling the level of NAD+ and the activity of Sirt1 in the heart and the cardiomyocytes therein. Nampt protects the heart from ischemia and reperfusion injury by stimulating Sirt1. In this review, we summarize what is currently known regarding the function of Nampt in the heart. (C) 2014 Elsevier B.V. All rights reserved.
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