NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential.
NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential.
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NAD〜代谢：病理生理机制和治疗潜力
DOI：
10.1038/s41392-020-00311-7
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发表时间：
2020-10-07
影响因子：
39.3
通讯作者：
Zou B
中科院分区：
文献类型：
--
作者：
Xie N;Zhang L;Gao W;Huang C;Huber PE;Zhou X;Li C;Shen G;Zou B
烟酰胺腺嘌呤二核苷酸（NAD+）及其代谢产物作为维持生理过程的关键调节剂，使可塑性细胞能够适应环境变化，包括营养扰动、遗传毒性因素、昼夜节律紊乱、感染、炎症和外源性物质。这些作用主要通过NAD+作为酶辅因子在氧化还原反应中转移氢对代谢途径的驱动作用来实现。此外，多种NAD+依赖性酶通过DNA、RNA和蛋白质的合成后化学修饰或释放第二信使环状ADP-核糖（cADPR）和NAADP+参与生理。NAD+代谢的长期失衡扰乱了生理功能，导致包括代谢疾病、癌症、衰老和神经退行性疾病在内的疾病。在这篇综述中，我们总结了最近的进展，在我们的理解NAD+调节应激生理反应的分子机制，通过操纵细胞通讯网络的NAD+缺乏对各种疾病的贡献和潜在的新途径的治疗干预。
Nicotinamide adenine dinucleotide (NAD+) and its metabolites function as critical regulators to maintain physiologic processes, enabling the plastic cells to adapt to environmental changes including nutrient perturbation, genotoxic factors, circadian disorder, infection, inflammation and xenobiotics. These effects are mainly achieved by the driving effect of NAD+ on metabolic pathways as enzyme cofactors transferring hydrogen in oxidation-reduction reactions. Besides, multiple NAD+-dependent enzymes are involved in physiology either by post-synthesis chemical modification of DNA, RNA and proteins, or releasing second messenger cyclic ADP-ribose (cADPR) and NAADP+. Prolonged disequilibrium of NAD+ metabolism disturbs the physiological functions, resulting in diseases including metabolic diseases, cancer, aging and neurodegeneration disorder. In this review, we summarize recent advances in our understanding of the molecular mechanisms of NAD+-regulated physiological responses to stresses, the contribution of NAD+ deficiency to various diseases via manipulating cellular communication networks and the potential new avenues for therapeutic intervention.
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影响因子：
5.7
作者：
Abu Aboud O;Chen CH;Senapedis W;Baloglu E;Argueta C;Weiss RH
通讯作者：
Weiss RH
DOI：
10.1126/science.1211485
发表时间：
2011-12-02
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Anastasiou D;Poulogiannis G;Asara JM;Boxer MB;Jiang JK;Shen M;Bellinger G;Sasaki AT;Locasale JW;Auld DS;Thomas CJ;Vander Heiden MG;Cantley LC
通讯作者：
Cantley LC
影响因子：
4.8
作者：
Ando, Hitoshi;Kumazaki, Masafumi;Fujimura, Akio
通讯作者：
Fujimura, Akio
影响因子：
29
作者：
Anderson KA;Huynh FK;Fisher-Wellman K;Stuart JD;Peterson BS;Douros JD;Wagner GR;Thompson JW;Madsen AS;Green MF;Sivley RM;Ilkayeva OR;Stevens RD;Backos DS;Capra JA;Olsen CA;Campbell JE;Muoio DM;Grimsrud PA;Hirschey MD
通讯作者：
Hirschey MD
影响因子：
8
作者：
Ariumi, Y;Masutani, M;Noda, M
通讯作者：
Noda, M