title: Mitochondrial biogenesis in kidney disease.
abstract: The transcriptional regulation of mitochondrial biogenesis by normal metabolic adaptation or injury has been clarified over the past decade. Mitochondrial biogenesis and its attendant processes enhance metabolic pathways such as fatty acid oxidation and increase antioxidant defense mechanisms that ameliorate injury from aging, tissue hypoxia, and glucose or fatty acid overload, all of which contribute to the pathogenesis of acute and chronic kidney disease. There has been considerable interest in peroxisome proliferator-activated receptors (PPAR) in the kidney, which affect multiple processes in addition to mitochondrial biogenesis. As yet there is relatively little information focused specifically on mitochondrial biogenesis and its regulation by PPARγ coactivators and their modulators such as SIRT1. The available data indicate that these pathways will be fruitful areas for study in the modification of renal disease.
authors.affiliation: Nephrology Division, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-5676, USA. wnberg@umich.edu
authors.forename: Joel M
authors.initials: JM
authors.lastname: Weinberg
mesh_terms: D005227:Fatty Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007674:Kidney Diseases / Q000503:physiopathology*; D008928:Mitochondria / Q000502:physiology*; D047495:PPAR gamma / Q000502:physiology; D056564:Sirtuin 1 / Q000502:physiology
chemical_list: D005227:Fatty Acids; D047495:PPAR gamma; C447939:SIRT1 protein, human; D056564:Sirtuin 1; D005947:Glucose