局灶节段性肾小球硬化中的瘢痕形成机制
Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.
作者信息
Sun Ke, Xie Qionghong, Hao Chuan-Ming
机构信息
Division of Nephrology, Huashan Hospital, Fudan University, Shanghai, China.
Nephrology Division, Vanderbilt University Medical Center School of Medicine, Nashville, Tennessee, USA.
出版信息
Kidney Dis (Basel). 2021 Sep;7(5):350-358. doi: 10.1159/000517108. Epub 2021 Jul 2.
BACKGROUND
Focal segmental glomerulosclerosis (FSGS) is a histologic pattern characterized by focal glomerular scarring, which often progresses to systemic and diffuse glomerulosclerosis. Previous studies have emphasized that the initiation of classic FSGS occurs in podocytes. The dysfunction and loss of podocytes have been associated with the development of proteinuria and the progression of various diseases. In addition, primary, secondary, and genetic FSGS are caused by different mechanisms of podocyte injury.
SUMMARY
The potential sources and mechanism of podocyte supplementation are the focus of our current research. Increasing attention has been paid to the role played by parietal epithelial cells (PECs) during the progression of FSGS. PECs are not only the primary influencing factors in glomerulosclerosis lesions but also have repair abilities, which remain a focus of debate. Notably, other resident glomerular cells also play significant roles in the progression of this disease.
KEY MESSAGE
In this review, we focus on the mechanism of scarring in FSGS and discuss current and potential therapeutic strategies.
背景
局灶节段性肾小球硬化（FSGS）是一种以局灶性肾小球瘢痕形成为特征的组织学模式，常进展为全身性和弥漫性肾小球硬化。既往研究强调经典FSGS始于足细胞。足细胞的功能障碍和丢失与蛋白尿的发生及各种疾病的进展有关。此外，原发性、继发性和遗传性FSGS由不同的足细胞损伤机制引起。
总结
足细胞补充的潜在来源和机制是我们当前研究的重点。壁层上皮细胞（PEC）在FSGS进展过程中所起的作用受到越来越多的关注。PEC不仅是肾小球硬化病变的主要影响因素，还具有修复能力，这仍是一个有争议的焦点。值得注意的是，其他肾小球固有细胞在该疾病的进展中也起重要作用。
关键信息
在本综述中，我们聚焦于FSGS的瘢痕形成机制，并讨论当前及潜在的治疗策略。
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