线粒体生物发生
生物发生
过氧化物酶体增殖物激活受体
过氧化物酶体
线粒体
细胞生物学
生物
肾脏疾病
β氧化
受体
内分泌学
脂肪酸
生物化学
基因
出处
期刊:Journal of The American Society of Nephrology
日期:2011-02-26
卷期号:22 (3): 431-436
被引量:116
标识
DOI:10.1681/asn.2010060643
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 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.
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