Mitochondrial Biogenesis in Kidney Disease

被引:114
作者
Weinberg, Joel M. [1 ,2 ]
机构
[1] Univ Michigan, Med Ctr, Div Nephrol, Dept Internal Med, Ann Arbor, MI 48109 USA
[2] Vet Affairs Ann Arbor Healthcare Syst, Div Nephrol, Dept Internal Med, Ann Arbor, MI USA
来源
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2011年 / 22卷 / 03期
基金
美国国家卫生研究院;
关键词
NITRIC-OXIDE SYNTHASE; PPAR-ALPHA; TRANSCRIPTIONAL CONTROL; HEME OXYGENASE-1; PGC-1-ALPHA EXPRESSION; ENERGY HOMEOSTASIS; GENE-TRANSCRIPTION; COACTIVATOR; PROTECTS; METABOLISM;
D O I
10.1681/ASN.2010060643
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
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 PPAR gamma 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.
引用
收藏
页码:431 / 436
页数:6
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