NAD+激酶
CD38
烟酰胺腺嘌呤二核苷酸
锡尔图因
PARP1
生物化学
聚ADP核糖聚合酶
西妥因1
化学
酶
生物
烟酰胺
细胞生物学
下调和上调
聚合酶
基因
干细胞
川地34
作者
Qiuzhen Lin,Wanyun Zuo,Yaozhong Liu,Keke Wu,Qiming Liu
标识
DOI:10.1016/j.cca.2021.01.012
摘要
Nicotinamide adenine dinucleotide (NAD) plays pivotal roles in controlling many biochemical processes. ‘NAD’ refers to the chemical backbone irrespective of charge, whereas ‘NAD+’ and ‘NADH’ refers to oxidized and reduced forms, respectively. NAD+/NADH ratio is essential for maintaining cellular reduction–oxidation (redox) homeostasis and for modulating energy metabolism. As a sensing or consuming enzyme of the poly (ADP-ribose) polymerase 1 (PARP1), the cyclic ADP-ribose (cADPR) synthases (CD38 and CD157), and sirtuin protein deacetylases (sirtuins, SIRTs), NAD+ participates in several key processes in cardiovascular disease. For example, NAD+ protects against metabolic syndrome, heart failure, ischemia–reperfusion (IR) injury, arrhythmia and hypertension. Accordingly, the subsequent loss of NAD+ in aging or during stress results in altered metabolic status and potentially increased disease susceptibility. Therefore, it is essential to maintain NAD+ or reduce loss in the heart. This review focuses on the involvement of NAD+ in the pathogenesis of cardiovascular disease and explores the effects of NAD+ boosting strategies in cardiovascular health.
科研通智能强力驱动
Strongly Powered by AbleSci AI