Abstract：
Podocytes are terminally differentiated kidney cells acting as the main gatekeepers of the glomerular filtration barrier; hence, inhibiting proteinuria. Podocytopathies are classified as kidney diseases caused by podocyte damage. Different genetic and environmental risk factors can cause podocyte damage and death. Recent evidence shows that mitochondrial dysfunction also contributes to podocyte damage. Understanding alterations in mitochondrial metabolism and function in podocytopathies and whether altered mitochondrial homeostasis/dynamics is a cause or effect of podocyte damage are issues that need in-depth studies. This review highlights the roles of mitochondria and their bioenergetics in podocytes. Then, factors/signalings that regulate mitochondria in podocytes are discussed. After that, the role of mitochondrial dysfunction is reviewed in podocyte injury and the development of different podocytopathies. Finally, the mitochondrial therapeutic targets are considered.
摘要：
足细胞是终末分化的肾细胞，是肾小球滤过屏障的主要看门人；因此，抑制蛋白尿。足细胞病变被归类为由足细胞损伤引起的肾脏疾病。不同的遗传和环境危险因素可导致足细胞损伤和死亡。最近的证据表明，线粒体功能障碍也有助于足细胞损伤。了解足细胞病变中线粒体代谢和功能的改变以及线粒体稳态/动力学改变是否是足细胞损伤的原因或影响是需要深入研究的问题。这篇综述强调了线粒体及其生物能量在足细胞中的作用。然后，讨论了调节足细胞线粒体的因素/信号。之后,综述了线粒体功能障碍在足细胞损伤和不同足细胞病变发展中的作用。最后,考虑线粒体治疗靶点。
