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Review
. 2019 Sep;67(9):623-632.
doi: 10.1369/0022155419850170. Epub 2019 May 22.

Mechanisms of Scarring in Focal Segmental Glomerulosclerosis

Jianyong Zhong  1   2 , Jacob B Whitman  1 , Hai-Chun Yang  1   2 , Agnes B Fogo  1   2
Affiliations
Review

Mechanisms of Scarring in Focal Segmental Glomerulosclerosis

Jianyong Zhong et al. J Histochem Cytochem. 2019 Sep.

Abstract

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.

Keywords: FSGS; chronic kidney disease; endothelial cell; extracellular matrix; fibrosis; parietal epithelial cell; podocyte; transforming growth factor beta; tubular epithelial cell.

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Conflict of interest statement

Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Adverse crosstalk among podocyte and other local cells in FSGS.
See this image and copyright information in PMC

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