Zuowei Pei, Peng Qu, Yaoxin Wu
Journal: International journal of medical sciences 2024;21(2):369-375
PMID: 38169534
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.
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