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Clinical Practice: Mini-Review

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PPARγ-Coactivator-1α, Nicotinamide Adenine Dinucleotide and Renal Stress Resistance

Poyan Mehr A.a · Parikh S.M.a, b

Author affiliations

aDivision of Nephrology and bCenter for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA

Corresponding Author

Dr. Samir M. Parikh

Beth Israel Deaconess Medical Center

330 Brookline Avenue, RN 330C

Boston, MA 02215 (USA)

E-Mail sparikh1@bidmc.harvard.edu

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Nephron 2017;137:253–255

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Abstract

With one of the highest mitochondrial densities in the body, the kidneys consume approximately 10% of total oxygen while constituting 0.5% of body mass. Renal respiration is linear to solute extraction, linking oxidative metabolism directly to tubular function. This fundamental role of mitochondria in renal health may become an “Achilles heel” under duress. Acute kidney injury (AKI) related to each major class of stressor - inflammation, ischemia, and toxins - exhibits early and prominent mitochondrial injury. The mitochondrial biogenesis regulator, PPARγ-coactivator-1α (PGC1α), may confer tubular protection against these stressors. Recent work proposes that renal PGC1α directly increases levels of nicotinamide adenine dinucleotide (NAD+), an essential co-factor for energy metabolism that has lately been proposed as an anti-aging factor. This mini-review summarizes recent studies on AKI, PGC1α, and NAD+ that identify a direct mechanism between the regulation of metabolic health and the ability to resist renal stressors.

© 2017 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Clinical Practice: Mini-Review

Received: March 13, 2017
Accepted: March 21, 2017
Published online: June 08, 2017
Issue release date: Published online first

Number of Print Pages: 3
Number of Figures: 1
Number of Tables: 0

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

For additional information: https://www.karger.com/NEF


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