Podocyte-Specific Sialylation-Deficient Mice Serve as a Model for Human FSGS

Volume: 30, Issue: 6, Pages: 1021 - 1035
Published: Apr 30, 2019
Abstract
The etiology of steroid-resistant nephrotic syndrome, which manifests as FSGS, is not completely understood. Aberrant glycosylation is an often underestimated factor for pathologic processes, and structural changes in the glomerular endothelial glycocalyx have been correlated with models of nephrotic syndrome. Glycans are frequently capped by sialic acid (Sia), and sialylation's crucial role for kidney function is well known. Human podocytes are...
Paper Details
Title
Podocyte-Specific Sialylation-Deficient Mice Serve as a Model for Human FSGS
Published Date
Apr 30, 2019
Volume
30
Issue
6
Pages
1021 - 1035
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