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Abstract：
Podocyte injury can disrupt the glomerular filtration barrier (GFB), leading to podocytopathies that emphasize podocytes as the glomerulus\'s key organizer. The coordinated cytoskeleton is essential for supporting the elegant structure and complete functions of podocytes. Therefore, cytoskeleton rearrangement is closely related to the pathogenesis of podocytopathies. In podocytopathies, the rearrangement of the cytoskeleton refers to significant alterations in a string of slit diaphragm (SD) and focal adhesion proteins such as the signaling node nephrin, calcium influx via transient receptor potential channel 6 (TRPC6), and regulation of the Rho family, eventually leading to the disorganization of the original cytoskeletal architecture. Thus, it is imperative to focus on these proteins and signaling pathways to probe the cytoskeleton rearrangement in podocytopathies. In this review, we describe podocytopathies and the podocyte cytoskeleton, then discuss the molecular mechanisms involved in cytoskeleton rearrangement in podocytopathies and summarize the effects of currently existing drugs on regulating the podocyte cytoskeleton.
摘要：
足细胞损伤可破坏肾小球滤过屏障（GFB），导致足细胞病，强调足细胞是肾小球的主要组织者。协调的细胞骨架对于支持足细胞的优雅结构和完整功能至关重要。因此,细胞骨架重排与足细胞病的发病机制密切相关。在足细胞病中，细胞骨架的重排是指一系列狭缝隔膜（SD）和粘着斑蛋白（如信号节点nephrin）的显着改变，钙通过瞬时受体电位通道6（TRPC6）流入，以及Rho家族的监管，最终导致原始细胞骨架结构的解体。因此，必须关注这些蛋白质和信号通路，以探索足细胞病变中的细胞骨架重排。在这次审查中,我们描述了足细胞病和足细胞细胞骨架，然后讨论了足细胞病变中细胞骨架重排的分子机制，并总结了现有药物对足细胞骨架的调控作用。
