SUN-190 GFB-887, a small molecule inhibitor of TRPC5, protects against podocyte injury and attenuates proteinuria in models of FSGS

P. MUNDEL, A. Westerling-Bui, M. Ledeboer, M. Coeffet-Le Gal, X.R. Pan-Zhou, M. Yu,M. Daniels, C. Plato,J.C. Harmange,J. Reilly

Kidney International Reports(2019)

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摘要
Focal segmental glomerulosclerosis (FSGS) is a rare podocytopathy with a high likelihood of progression to end stage renal disease. The Ca2+-permeable transient receptor potential canonical 5 (TRPC5) channel is a critical mediator of proteinuria in FSGS. Activation of the TRPC5 pathway in podocytes culminates in activation of Rac1, which is the primary driver of proteinuria in many forms of familial and sporadic FSGS. Inhibition of TRPC5 channel activity has been shown to protect against proteinuria and podocyte loss in AT1R transgenic and Dahl salt-sensitive rats.
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关键词
Focal Segmental Glomerulosclerosis
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