NAD+激酶
烟酰胺磷酸核糖转移酶
CD38
烟酰胺腺嘌呤二核苷酸
锡尔图因
生物
西妥因1
辅因子
生物化学
SIRT3
PARP1
聚ADP核糖聚合酶
酶
细胞生物学
聚合酶
川地34
下调和上调
基因
干细胞
作者
Shin‐ichiro Imai,Leonard Guarente
标识
DOI:10.1016/j.tcb.2014.04.002
摘要
Nicotinamide adenine dinucleotide (NAD(+)) is a classical coenzyme mediating many redox reactions. NAD(+) also plays an important role in the regulation of NAD(+)-consuming enzymes, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38/157 ectoenzymes. NAD(+) biosynthesis, particularly mediated by nicotinamide phosphoribosyltransferase (NAMPT), and SIRT1 function together to regulate metabolism and circadian rhythm. NAD(+) levels decline during the aging process and may be an Achilles' heel, causing defects in nuclear and mitochondrial functions and resulting in many age-associated pathologies. Restoring NAD(+) by supplementing NAD(+) intermediates can dramatically ameliorate these age-associated functional defects, counteracting many diseases of aging, including neurodegenerative diseases. Thus, the combination of sirtuin activation and NAD(+) intermediate supplementation may be an effective antiaging intervention, providing hope to aging societies worldwide.
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