NAD⁺-A Hub of Energy Metabolism in Heart Failure

Abstract

Heart failure is a condition where reduced levels of adenosine triphosphate (ATP) affect energy supply in myocardial cells. Nicotinamide adenine dinucleotide (NAD + ) plays a crucial role as a coenzyme for electron transfer in energy metabolism. Decreased NAD + levels in myocardial cells lead to inadequate ATP production and increased susceptibility to heart failure. Researchers are exploring ways to increase NAD + levels to alleviate heart failure. Targets such as sirtuin2 (sirt2), sirtuin3 (sirt3), Poly (ADP-ribose) polymerase (PARP), and diastolic regulatory proteins are being investigated. NAD + supplementation has shown promise, even in heart failure with preserved ejection fraction (HFpEF). By focusing on NAD + as a central component of energy metabolism, it is possible to improve myocardial activity, heart function, and address energy deficiency in heart failure.

The role of nicotinamide adenine dinucleotide salvage enzymes in cardioprotection

“…Extracellular NAMPT (eNAMPT) has emerged as a cytokine in pre-β-cell colony-enhancing factor (PBEF) that helps the maturation of β cells by activating Toll-like receptor 4 (TLR4) [ 36 ]. It was reported that pharmaceutically activated NAMPT in a diabetic mouse model decreased the NADH/NAD + ratio and improved overall cardiac function by improving p-AKT, p-eNOS, and Beclin 1 expression [ 37 ]. Overexpression of NAMPT can increase NAD + synthesis and ATP levels in cardiomyocytes to protect against myocardial injury due to in vitro myocardial ischemia and reperfusion [ 38 ].…”