
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.
Myocardium, Myocardial Ischemia, Cardiomegaly, Mice, Transgenic, Myocardial Reperfusion Injury, Gene Expression Regulation, Autophagy, Animals, Humans, Nicotinamide Phosphoribosyltransferase
Myocardium, Myocardial Ischemia, Cardiomegaly, Mice, Transgenic, Myocardial Reperfusion Injury, Gene Expression Regulation, Autophagy, Animals, Humans, Nicotinamide Phosphoribosyltransferase
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