Focal segmental glomerulosclerosis (FSGS) presents with scar in parts of some glomeruli and often progresses to global and diffuse glomerulosclerosis. Podocyte injury is the initial target in primary FSGS, induced by a circulating factor. Several gene variants, for example, APOL1, are associated with increased susceptibility to FSGS. Primary FSGS may be due to genetic mutation in key podocyte genes. Increased work stress after loss of nephrons, epigenetic mechanisms, and various profibrotic pathways can contribute to progressive sclerosis, regardless of the initial injury. The progression of FSGS lesions also involves crosstalk between podocytes and other kidney cells, such as parietal epithelial cells, glomerular endothelial cells, and even tubular epithelial cells. New insights related to these mechanisms could potentially lead to new therapeutic strategies to prevent progression of FSGS.

中文翻译：

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局灶节段性肾小球硬化症的疤痕形成机制。


局灶节段性肾小球硬化症 (FSGS) 表现为部分肾小球部分出现疤痕，并经常进展为整体性弥漫性肾小球硬化症。足细胞损伤是原发性 FSGS 的最初目标，由循环因子诱导。一些基因变异，例如 APOL1，与 FSGS 易感性增加有关。原发性 FSGS 可能是由于关键足细胞基因的基因突变所致。无论最初的损伤如何，肾单位、表观遗传机制和各种促纤维化途径丧失后的工作压力增加都可能导致进行性硬化。 FSGS 病变的进展还涉及足细胞与其他肾细胞（如壁上皮细胞、肾小球内皮细胞，甚至肾小管上皮细胞）之间的串扰。与这些机制相关的新见解可能会带来新的治疗策略来预防 FSGS 的进展。