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000163955 1001_ $$aXie, Na$$b0
000163955 245__ $$aNAD+ metabolism: pathophysiologic mechanisms and therapeutic potential.
000163955 260__ $$aLondon$$bMacmillan Publishers, part of Springer Nature$$c2020
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000163955 520__ $$aNicotinamide adenine dinucleotide (NAD+) and its metabolites function as critical regulators to maintain physiologic processes, enabling the plastic cells to adapt to environmental changes including nutrient perturbation, genotoxic factors, circadian disorder, infection, inflammation and xenobiotics. These effects are mainly achieved by the driving effect of NAD+ on metabolic pathways as enzyme cofactors transferring hydrogen in oxidation-reduction reactions. Besides, multiple NAD+-dependent enzymes are involved in physiology either by post-synthesis chemical modification of DNA, RNA and proteins, or releasing second messenger cyclic ADP-ribose (cADPR) and NAADP+. Prolonged disequilibrium of NAD+ metabolism disturbs the physiological functions, resulting in diseases including metabolic diseases, cancer, aging and neurodegeneration disorder. In this review, we summarize recent advances in our understanding of the molecular mechanisms of NAD+-regulated physiological responses to stresses, the contribution of NAD+ deficiency to various diseases via manipulating cellular communication networks and the potential new avenues for therapeutic intervention.
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000163955 7001_ $$aZhang, Lu$$b1
000163955 7001_ $$aGao, Wei$$b2
000163955 7001_ $$00000-0003-2247-7750$$aHuang, Canhua$$b3
000163955 7001_ $$0P:(DE-He78)3291aaac20f3d603d96744c1f0890028$$aHuber, Peter Ernst$$b4$$udkfz
000163955 7001_ $$aZhou, Xiaobo$$b5
000163955 7001_ $$aLi, Changlong$$b6
000163955 7001_ $$aShen, Guobo$$b7
000163955 7001_ $$0P:(DE-He78)288563599778a46193872ab022a9ce0f$$aZou, Bingwen$$b8$$eLast author$$udkfz
000163955 773__ $$0PERI:(DE-600)2886872-9$$a10.1038/s41392-020-00311-7$$gVol. 5, no. 1, p. 227$$n1$$p227$$tSignal transduction and targeted therapy$$v5$$x2059-3635$$y2020
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