SRT1720 induces mitochondrial biogenesis and rescues mitochondrial function after oxidant injury in renal proximal tubule cells.

The Journal of Pharmacology and Experimental Therapeutics
Jason A FunkRick G Schnellmann

Abstract

Mitochondrial biogenesis occurs under basal conditions and is an adaptive response initiated by cells to maintain energetic demands and metabolic homeostasis after injuries targeting mitochondrial function. Identifying pharmacological agents that stimulate mitochondrial biogenesis is a critical step in the development of new therapeutics for the treatment of these injuries and to test the hypothesis that these agents will expedite recovery of cell and organ function after acute organ injuries. In this study, we examined the effects of N-[2-[3-(piperazin-1-ylmethyl)imidazo[2,1-b][1,3]thiazol-6-yl]phenyl]quinoxaline-2-carboxamide (SRT1720) on mitochondrial biogenesis and function in primary cultures of renal proximal tubule cells (RPTCs). We also tested the ability of this compound to restore mitochondrial functions after oxidant-induced RPTC injury. SRT1720 (3-10 microM) induced mitochondrial biogenesis in RPTCs within 24 h as determined by elevations in mitochondrial DNA copy number, increased expression of the mitochondrial proteins NADH dehydrogenase 1beta subcomplex subunit 8 (NDUFB8) and ATP synthase beta, and elevated mitochondrial respiration rates and ATP levels. Induction of mitochondrial biogenesis depended on mammalia...Continue Reading

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