Open AccessThe Calcium-Dependent Protease Calpain-1 Links TRPC6 Activity to Podocyte Injury
Author(s) -
Kim A.T. Verheijden,
Ramon Sonneveld,
Marinka Bakker-van Bebber,
Jack F.M. Wetzels,
Johan van der Vlag,
Tom Nijenhuis
Publication year - 2018
Publication title -
journal of the american society of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.451
H-Index - 279
eISSN - 1533-3450
pISSN - 1046-6673
DOI - 10.1681/asn.2016111248
Subject(s) - trpc6 , calpain , podocyte , calcineurin , nephrin , microbiology and biotechnology , slit diaphragm , podocin , endocrinology , medicine , chemistry , biology , kidney , receptor , proteinuria , transplantation , biochemistry , transient receptor potential channel , enzyme
The hallmark of podocytopathies, such as FSGS, is podocyte injury resulting in proteinuria. Transient receptor potential channel C6 (TRPC6) is a calcium-conducting ion channel expressed at the slit diaphragm. TRPC6 gain-of-function mutations and glomerular TRPC6 overexpression are associated with proteinuria. However, the pathways linking TRPC6 to podocyte injury, which is characterized by loss of the slit diaphragm protein nephrin, activation of several intracellular pathways (including calcineurin-NFAT signaling), and cytoskeletal rearrangement, remain elusive.
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