Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 314, Issue 4, Pages H839-H852Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00409.2017
Keywords
cardiovascular diseases; ischemia-reperfusion; nicotinamide adenine dinucleotide; oxidation-reduction (redox)
Funding
- National Institutes of Health (NIH) [R01-HL-115955]
- American Heart Association Predoctoral Fellowship [17PRE33410450]
- NIH-supported Medical Scientist Training Program at the University of Iowa (NIH Grant) [T32-GM007337]
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Nicotinamide adenine dinucleotide (NAD(+)) and related metabolites are central mediators of fuel oxidation and bioenergetics within cardiomyocytes. Additionally, NAD(+) is required for the activity of multifunctional enzymes, including sirtuins and poly(ADP-ribose) polymerases that regulate posttranslational modifications, DNA damage responses, and Ca2+ signaling. Recent research has indicated that NAD(+) participates in a multitude of processes dysregulated in cardiovascular diseases. Therefore, supplementation of NAD(+) precursors, including nicotinamide riboside that boosts or repletes the NAD(+) metabolome, may be cardioprotective. This review examines the molecular physiology and preclinical data with respect to NAD(+) precursors in heart failure-related cardiac remodeling, ischemic-reperfusion injury, and arrhythmias. In addition, alternative NAD(+)-boosting strategies and potential systemic effects of NAD(+) supplementation with implications on cardiovascular health and disease are surveyed.
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