Full Text | PDF

Int J Med Sci 2024; 21(2):369-375. doi:10.7150/ijms.89370 This issue Cite

Review

NAD⁺-A Hub of Energy Metabolism in Heart Failure

Yaoxin Wu¹, Zuowei Pei^1,2✉, Peng Qu^1✉

1. Faculty of Medicine, Dalian University of Technology, 116024, Dalian, China.
2. Department of Cardiology, Central Hospital of Dalian University of Technology, Dalian, 116033, China.

✉ Corresponding authors: Peng Qu, Faculty of Medicine, Dalian University of Technology, 116024, Dalian, China. Telephone number: 0411-84706670. E-mail: qupengedu.cn. Zuowei Pei, Department of Cardiology, Central Hospital of Dalian University of Technology, No.826 Xinan Road, 116033, Dalian, China. Telephone number: +86-0411-84412001, Fax number: +86-0411-84412001. E-mail: pzw_dlcom. More

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.

Keywords: NAD⁺, Energy Metabolism, Heart Failure, Mitochondria

Citation styles

©2024 Ivyspring International Publisher. Terms of use