Department of Nephrology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Kidney Int. 2012 Oct;82(7):735-6. doi: 10.1038/ki.2012.182.
Dysfunction of mitochondria in podocytes is believed to be a trigger of injury and contributes to progressive glomerular sclerosis; however, the mechanisms had not been fully understood. Yuan et al. report involvement of SIRT1 (a homolog of the life-extending gene sir2 in mammals) and PPAR-γ coactivator 1α, a major regulator of oxidative metabolism, in mitochondria during podocyte injury. This information will be important in exploration of the mechanisms and future treatment of glomerular sclerosis.
足细胞中线粒体功能障碍被认为是损伤的触发因素，并导致进行性肾小球硬化；然而，其机制尚未完全阐明。袁等人报道了 SIRT1（哺乳动物中延长寿命基因 sir2 的同源物）和过氧化物酶体增殖物激活受体-γ共激活因子 1α（氧化代谢的主要调节剂）在足细胞损伤过程中参与线粒体的作用。这些信息对于探索肾小球硬化的机制和未来的治疗方法将是重要的。
