Journal
NATURE REVIEWS NEPHROLOGY
Volume 13, Issue 4, Pages 213-225Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrneph.2017.5
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Funding
- American Heart Association [12SDG8840004, 12IRG9010008]
- Ellison Medical Foundation
- Friedreich's Ataxia Research Alliance
- NIH [1F31HL127959, 1F31HL123275-31]
- NIA [R01AG045351]
- NIAAA [R01AA022146]
- National Institute of Ageing [P30AG028716-01]
- Duke O'Brien Center for Kidney Research [5P30DK096493-02]
- NIH/NIGMS [5T32GM007105-40]
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The coenzyme nicotinamide adenine dinucleotide (NAD(+)) has key roles in the regulation of redox status and energy metabolism. NAD(+) depletion is emerging as a major contributor to the pathogenesis of cardiac and renal diseases and NAD(+) repletion strategies have shown therapeutic potential as a means to restore healthy metabolism and physiological function. The pleotropic roles of NAD(+) enable several possible avenues by which repletion of this coenzyme could have therapeutic efficacy. In particular, NAD(+) functions as a co-substrate in deacylation reactions carried out by the sirtuin family of enzymes. These NAD(+)- dependent deacylases control several aspects of metabolism and a wealth of data suggests that boosting sirtuin activity via NAD+ supplementation might be a promising therapy for cardiac and renal pathologies. This Review summarizes the role of NAD(+) metabolism in the heart and kidney, and highlights the mitochondrial sirtuins as mediators of some of the beneficial effects of NAD(+)-boosting therapies in preclinical animal models. We surmise that modulating the NAD(+)-sirtuin axis is a clinically relevant approach to develop new therapies for cardiac and renal diseases.
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