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Metabolism. 2016 Apr;65(4):454-62. doi: 10.1016/j.metabol.2015.11.010. Epub 2015 Dec 1.

The potential regulatory roles of NAD(+) and its metabolism in autophagy.

Author information

1
Institute of Burn Research, Southwest Hospital, Third Military Medical University, State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing, PR China, 400038.
2
Endocrinology Department, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing, PR China, 400038.
3
Institute of Burn Research, Southwest Hospital, Third Military Medical University, State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing, PR China, 400038. Electronic address: yshuangtmmu@163.com.

Abstract

(Macro)autophagy mediates the bulk degradation of defective organelles, long-lived proteins and protein aggregates in lysosomes and plays a critical role in cellular and tissue homeostasis. Defective autophagy processes have been found to contribute to a variety of metabolic diseases. However, the regulatory mechanisms of autophagy are not fully understood. Increasing data indicate that nicotinamide adenine nucleotide (NAD(+)) homeostasis correlates intimately with autophagy. NAD(+) is a ubiquitous coenzyme that functions primarily as an electron carrier of oxidoreductase in multiple redox reactions. Both NAD(+) homeostasis and its metabolism are thought to play critical roles in regulating autophagy. In this review, we discuss how the regulation of NAD(+) and its metabolism can influence autophagy. We focus on the regulation of NAD(+)/NADH homeostasis and the effects of NAD(+) consumption by poly(ADP-ribose) (PAR) polymerase-1 (PARP-1), NAD(+)-dependent deacetylation by sirtuins and NAD(+) metabolites on autophagy processes and the underlying mechanisms. Future studies should provide more direct evidence for the regulation of autophagy processes by NAD(+). A better understanding of the critical roles of NAD(+) and its metabolites on autophagy will shed light on the complexity of autophagy regulation, which is essential for the discovery of new therapeutic tools for autophagy-related diseases.

KEYWORDS:

Autophagy; Ca(2)(+); NAADP/cADPR/ADPR; NAD(+); NAD(P)(+)/NAD(P)H

PMID:
26975537
DOI:
10.1016/j.metabol.2015.11.010
[Indexed for MEDLINE]

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