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Sensitizing the Slit Diaphragm with TRPC6 Ion Channels

Clemens C. Möller^*, Jan Flesche^* and Jochen Reiser^*,

^* Department of Medicine, Program in Glomerular Disease and Nephrology Division, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; and Division of Nephrology and Hypertension, Leonard Miller School of Medicine, University of Miami, Miami, Florida

Correspondence: Dr. Jochen Reiser, Division of Nephrology and Hypertension, Leonard Miller School of Medicine, University of Miami, 1120 NW 14th Street, Suite 1182 CRB C-211, Miami, FL 33136. Phone: 305-243-2349; Fax: 305-243-3506; E-mail: jreiser{at}med.miami.edu

Physiologic permeability of the glomerular capillary depends on the normal structure of podocyte foot processes forming a functioning slit diaphragm in between. Mutations in several podocyte genes as well as specific molecular pathways have been identified as the cause for progressive kidney failure with urinary protein loss. Podocyte injury is a hallmark of glomerular disease, which is generally displayed by the rearrangement of the podocyte slit diaphragm and the actin cytoskeleton. Recent studies demonstrate a unique role for the Ca²⁺-permeable ion channel protein TRPC6 as a regulator of glomerular ultrafiltration. In both genetic and acquired forms of proteinuric kidney disease, dysregulation of podocyte TRPC6 plays a pathogenic role. This article illustrates how recent findings add to emerging concepts in podocyte biology, particularly mechanosensation and signaling at the slit diaphragm.

Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673