足细胞损伤是FSGS发生的基础，SIRT1/PGC-1α介导的线粒体合成功能降低和SIRT1/FoxO3/BNIP3介导的线粒体自噬活动减弱是足细胞损伤的重要原因。益气化瘀清热方疗效确切，并可通过调节足细胞瞬时受体电位阳离子通道蛋白（TRPC6）和骨架蛋白podocin、 podocalyxin表达起到保护足细胞的作用。最新报道这一过程与线粒体自噬和合成有关，由此我们提出益气化瘀清热方可能通过调节SIRT1介导的SIRT1/PGC-1α线粒体合成及SIRT1/FoxO3/BNIP3线粒体自噬以阻止FSGS发生发展这一科学假说。本研究将从体内和体外两方面，通过siRNA技术分别阻断上述两个通路，检测通路关键因子及线粒体形态、数量、呼吸功能、代谢相关基因、线粒体DNA拷贝数、自噬相关指标、线粒体自噬体、足细胞自噬水平的变化情况，探讨上述通路在足细胞损伤中的机制，并揭示益气化瘀清热方的疗效机制。

Podocyte injury is the basis of the occurrence of FSGS. The decrease of mitochondrial synthesis function mediated by SIRT1/PGC-1α and the weakening of mitochondrial autophagy mediated by SIRT1/FoxO3/BNIP3 are important causes of podocyte injury. YiQi Huayu Qingre Decoction has a definite therapeutic effect. This decoction can play a role in protecting podocyte by regulating the expression of podocyte transient receptor potential cation channel protein (TRPC6), cytoskeleton protein podocin and podocalyxin. The latest report shows that this protection mechanism is related to mitochondrial autophagy and synthesis. Therefore, we propose a scientific hypothesis that Yiqi Huayu Qingre Decoction may prevent the development of FSGS by regulating SIRT1-mediated mitochondrial synthesis of SIRT1 / PGC-1α and mitochondrial autophagy of SIRT1 / FoxO3 / BNIP3. In this study, the above two pathways will be blocked by siRNA technology both in vivo and in vitro to research the mechanism of the above two pathways in podocyte injury and explore the therapeutic mechanism of Yiqi Huayu Qingre Decoction. Therefore, a lot of evaluation indicators will be detected, such as the key indicators of the above pathways, and mitochondrial morphology, number, respiratory function, metabolism-related genes, mitochondrial DNA copy number, autophagy-related indicators, mitochondrial autonomy. And also the changes in the level of autophagy in podocytes will be researched.