Nephrology Division, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-5676, USA.
J Am Soc Nephrol. 2011 Mar;22(3):431-6. doi: 10.1681/ASN.2010060643. Epub 2011 Feb 25.
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.
过去十年中，人们已经阐明了正常代谢适应或损伤对线粒体生物发生的转录调控。线粒体生物发生及其伴随的过程增强了代谢途径，如脂肪酸氧化，并增加了抗氧化防御机制，从而减轻了衰老、组织缺氧以及葡萄糖或脂肪酸过载引起的损伤，所有这些都促成了急性和慢性肾脏病的发病机制。过氧化物酶体增殖物激活受体 (PPAR) 在肾脏中引起了相当大的兴趣，除了线粒体生物发生之外，它还影响多种过程。到目前为止，关于线粒体生物发生及其受 PPARγ 共激活因子及其调节剂（如 SIRT1）的调节的具体信息相对较少。现有数据表明，这些途径将是肾脏病修饰研究的富有成果的领域。
