Role of nicotinamide adenine dinucleotide in cardiovascular disease

Purpose of review The nicotinamide adenine dinucleotide (NAD + ) is an important redox cofactor that plays a major role in energy metabolism. This review provides an overview of the current understanding of NAD + in cardiovascular diseases. Recent findings Activation of the rate-limiting enzyme nicotinamide phosphoribosyltransferase (NAMPT), a key component of the NAD + salvage pathway, is emerging as an alternative method to replenish the cycling NAD + pools and to alleviate the cardiovascular pathophysiology driven by NAD + depletion. The NAD + -dependent sirtuins play an important role in cellular metabolism and integrate the circadian signaling of clock controlled Nampt oscillation and thereby NAD + synthesis. Summary An imbalance in the NAD + /NADH ratio caused by NAD + depletion is implicated in various diseases, including metabolic disease, aging, and cancer. The cellular NAD + content is decreased in cardiovascular diseases and heart failure. Lack of NAD + in cardiomyocytes leads to mitochondrial dysfunction, increased reactive oxygen species (ROS) production and cell death. The supplementation of NAD + and its precursors such as nicotinic acid (NA), nicotinamide (NAM), nicotinamide mononucleotide (NMN), and nicotinamide riboside (NR) are currently being evaluated in clinical trials. This review mainly focuses on the role of NAD + in cardiovascular diseases and therapeutics.