PGC1α drives NAD biosynthesis linking oxidative metabolism to renal protection

Mei T. Tran, Zsuzsanna K. Zsengeller, Anders H. Berg, Eliyahu V. Khankin, Manoj K. Bhasin, Wondong Kim, Clary B. Clish, Isaac E. Stillman, S. Ananth Karumanchi, Eugene P. Rhee and Samir M. Parikh ()
Additional contact information
Mei T. Tran: Beth Israel Deaconess Medical Center and Harvard Medical School
Zsuzsanna K. Zsengeller: Beth Israel Deaconess Medical Center and Harvard Medical School
Anders H. Berg: Beth Israel Deaconess Medical Center and Harvard Medical School
Eliyahu V. Khankin: Beth Israel Deaconess Medical Center and Harvard Medical School
Manoj K. Bhasin: Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School
Wondong Kim: Massachusetts General Hospital and Harvard Medical School
Clary B. Clish: Broad Institute of MIT and Harvard
Isaac E. Stillman: Beth Israel Deaconess Medical Center and Harvard Medical School
S. Ananth Karumanchi: Beth Israel Deaconess Medical Center and Harvard Medical School
Eugene P. Rhee: Massachusetts General Hospital and Harvard Medical School
Samir M. Parikh: Beth Israel Deaconess Medical Center and Harvard Medical School

Nature, 2016, vol. 531, issue 7595, 528-532

Abstract: PGC1α protects against kidney injury by upregulating enzymes that enhance nicotinamide adenine dinucleotide (NAD) and driving local accumulation of the fatty acid breakdown product β-hydroxybutyrate, which leads to increased production of the renoprotective prostaglandin E2.

Date: 2016
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DOI: 10.1038/nature17184

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