Faculty Collaboration Database

TRPC6 channel as an emerging determinant of the podocyte injury susceptibility in kidney diseases. Am J Physiol Renal Physiol 2015 Sep 01;309(5):F393-7

Date

06/19/2015

Pubmed ID

26084930

Pubmed Central ID

PMC4556891

DOI

10.1152/ajprenal.00186.2015

Scopus ID

2-s2.0-84940840071 (requires institutional sign-in at Scopus site)   106 Citations

Abstract

Podocytes (terminally differentiated epithelial cells of the glomeruli) play a key role in the maintenance of glomerular structure and permeability and in the incipiency of various renal abnormalities. Injury to podocytes is considered a major contributor to the development of kidney disease as their loss causes proteinuria and progressive glomerulosclerosis. The physiological function of podocytes is critically dependent on proper intracellular calcium handling; excessive calcium influx in these cells may result in the effacement of foot processes, apoptosis, and subsequent glomeruli damage. One of the key proteins responsible for calcium flux in the podocytes is transient receptor potential cation channel, subfamily C, member 6 (TRPC6); a gain-of-function mutation in TRPC6 has been associated with the onset of the familial forms of focal segmental glomerulosclerosis (FSGS). Recent data also revealed a critical role of this channel in the onset of diabetic nephropathy. Therefore, major efforts of the research community have been recently dedicated to unraveling the TRPC6-dependent effects in the initiation of podocyte injury. This mini-review focuses on the TRPC6 channel in podocytes and colligates recent data in an attempt to shed some light on the mechanisms underlying the pathogenesis of TRPC6-mediated glomeruli damage and its potential role as a therapeutic target for the treatment of chronic kidney diseases.

Author List

Ilatovskaya DV, Staruschenko A

MESH terms used to index this publication - Major topics in bold

Diabetic Nephropathies
Disease Susceptibility
Glomerulosclerosis, Focal Segmental
Humans
Kidney Diseases
Mutation
Podocytes
Signal Transduction
TRPC Cation Channels
TRPC6 Cation Channel