Literature DB >> 17346947

TRP channels in kidney disease.

Yu-Juei Hsu1, Joost G J Hoenderop, René J M Bindels.   

Abstract

Mammalian TRP channel proteins form six-transmembrane cation-permeable channels that may be grouped into six subfamilies on the basis of amino acid sequence homology (TRPC, TRPV, TRPM, TRPA, TRPP, and TRPML). Recent studies of TRP channels indicate that they are involved in numerous fundamental cell functions and are considered to play an important role in the pathophysiology of many diseases. Many TRPs are expressed in kidney along different parts of the nephron and growing evidence suggest that these channels are involved in hereditary, as well as acquired kidney disorders. TRPC6, TRPM6, and TRPP2 have been implicated in hereditary focal segmental glomerulosclerosis (FSGS), hypomagnesemia with secondary hypocalcemia (HSH), and polycystic kidney disease (PKD), respectively. In addition, the highly Ca(2+)-selective channel, TRPV5, contributes to several acquired mineral (dys)regulation, such as diabetes mellitus (DM), acid-base disorders, diuretics, immunosuppressant agents, and vitamin D analogues-associated Ca(2+) imbalance whereas TRPV4 may function as an osmoreceptor in kidney and participate in the regulation of sodium and water balance. This review presents an overview of the current knowledge concerning the distribution of TRP channels in kidney and their possible roles in renal physiology and kidney diseases.

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Year:  2007        PMID: 17346947     DOI: 10.1016/j.bbadis.2007.02.001

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


  19 in total

1.  Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathway.

Authors:  Tom Nijenhuis; Alexis J Sloan; Joost G J Hoenderop; Jan Flesche; Harry van Goor; Andreas D Kistler; Marinka Bakker; Rene J M Bindels; Rudolf A de Boer; Clemens C Möller; Inge Hamming; Gerjan Navis; Jack F M Wetzels; Jo H M Berden; Jochen Reiser; Christian Faul; Johan van der Vlag
Journal:  Am J Pathol       Date:  2011-08-11       Impact factor: 4.307

Review 2.  Canonical transient receptor potential channels in diabetes.

Authors:  Sarabeth Graham; Joseph P Yuan; Rong Ma
Journal:  Exp Biol Med (Maywood)       Date:  2012-01-26

3.  When EGF is offside, magnesium is wasted.

Authors:  Shmuel Muallem; Orson W Moe
Journal:  J Clin Invest       Date:  2007-08       Impact factor: 14.808

Review 4.  Distal convoluted tubule.

Authors:  James A McCormick; David H Ellison
Journal:  Compr Physiol       Date:  2015-01       Impact factor: 9.090

5.  TRPC6 G757D Loss-of-Function Mutation Associates with FSGS.

Authors:  Marc Riehle; Anja K Büscher; Björn-Oliver Gohlke; Mario Kaßmann; Maria Kolatsi-Joannou; Jan H Bräsen; Mato Nagel; Jan U Becker; Paul Winyard; Peter F Hoyer; Robert Preissner; Dietmar Krautwurst; Maik Gollasch; Stefanie Weber; Christian Harteneck
Journal:  J Am Soc Nephrol       Date:  2016-02-18       Impact factor: 10.121

Review 6.  TRP channels and their implications in metabolic diseases.

Authors:  Zhiming Zhu; Zhidan Luo; Shuangtao Ma; Daoyan Liu
Journal:  Pflugers Arch       Date:  2010-11-26       Impact factor: 3.657

7.  The novel role of TRPC6 in vitamin D ameliorating podocyte injury in STZ-induced diabetic rats.

Authors:  Xiaoliang Zhang; Zhixia Song; Yinfeng Guo; Min Zhou
Journal:  Mol Cell Biochem       Date:  2014-10-09       Impact factor: 3.396

8.  Evidence for the functional involvement of members of the TRP channel family in the uptake of Na(+) and NH4 (+) by the ruminal epithelium.

Authors:  Julia Rosendahl; Hannah S Braun; Katharina T Schrapers; Holger Martens; Friederike Stumpff
Journal:  Pflugers Arch       Date:  2016-05-17       Impact factor: 3.657

9.  A simple spectrofluorometric assay to measure total intracellular magnesium by a hydroxyquinoline derivative.

Authors:  Giovanna Farruggia; Stefano Iotti; Luca Prodi; Nelsi Zaccheroni; Marco Montalti; Paul B Savage; Giulia Andreani; Valentina Trapani; Federica I Wolf
Journal:  J Fluoresc       Date:  2008-06-05       Impact factor: 2.217

10.  A novel TRPC6 mutation that causes childhood FSGS.

Authors:  Saskia F Heeringa; Clemens C Möller; Jianyang Du; Lixia Yue; Bernward Hinkes; Gil Chernin; Christopher N Vlangos; Peter F Hoyer; Jochen Reiser; Friedhelm Hildebrandt
Journal:  PLoS One       Date:  2009-11-10       Impact factor: 3.240

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