A background Ca2+ entry pathway mediated by TRPC1/TRPC4 is critical for development of pathological cardiac remodelling.

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Abstract

Pathological cardiac hypertrophy is a major predictor for the development of cardiac diseases. It is associated with chronic neurohumoral stimulation and with altered cardiac Ca(2+) signalling in cardiomyocytes. TRPC proteins form agonist-induced cation channels, but their functional role for Ca(2+) homeostasis in cardiomyocytes during fast cytosolic Ca(2+) cycling and neurohumoral stimulation leading to hypertrophy is unknown.

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Journal

Journal ID (iso-abbrev): Eur. Heart J.

Title: European heart journal

Publisher: Oxford University Press (OUP)

ISSN (Electronic): 1522-9645

ISSN (Print): 0195-668X

Publication date (Electronic): Sep 01 2015

Volume: 36

Issue: 33

Affiliations

[1 ] Pharmakologisches Institut, Ruprecht-Karls-Universität Heidelberg, 69120 Heidelberg, Germany Experimentelle und Klinische Pharmakologie und Toxikologie, 66421 Homburg, Germany DZHK (German Centre for Cardiovascular Research), partner site Heidelberg/Mannheim, Germany.

[2 ] Institut für Molekulare Zellbiologie, 66421 Homburg, Germany.

[3 ] Experimentelle und Klinische Pharmakologie und Toxikologie, 66421 Homburg, Germany.

[4 ] Innere Medizin III Universität des Saarlandes, 66421 Homburg, Germany.

[5 ] DZHK (German Centre for Cardiovascular Research), partner site Heidelberg/Mannheim, Germany Research Unit Cardiac Epigenetics, Department of Cardiology, Ruprecht-Karls-Universität Heidelberg, 69120 Heidelberg, Germany Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 430030 Wuhan, China.

[6 ] Pharmakologisches Institut, Ruprecht-Karls-Universität Heidelberg, 69120 Heidelberg, Germany Experimentelle und Klinische Pharmakologie und Toxikologie, 66421 Homburg, Germany.

[7 ] Institut für Physiologie, Universität Regensburg, 93053 Regensburg, Germany.

[8 ] Walther-Straub-Institut für Pharmakologie und Toxikologie, LMU, 80336 München, Germany.

[9 ] Transmembrane Signaling Group, NIEHS, PO Box 12233, NC 27709, USA.

[10 ] Pharmakologisches Institut, Ruprecht-Karls-Universität Heidelberg, 69120 Heidelberg, Germany Experimentelle und Klinische Pharmakologie und Toxikologie, 66421 Homburg, Germany DZHK (German Centre for Cardiovascular Research), partner site Heidelberg/Mannheim, Germany marc.freichel@pharma.uni-heidelberg.de peter.lipp@uniklinikum-saarland.de.

[11 ] Institut für Molekulare Zellbiologie, 66421 Homburg, Germany marc.freichel@pharma.uni-heidelberg.de peter.lipp@uniklinikum-saarland.de.

Article

Publisher Item ID: ehv250

DOI: 10.1093/eurheartj/ehv250

PMC ID: 4554959

PubMed ID: 26069213

SO-VID: 3916366f-795f-4a20-91b0-0332f5246098

History

Keywords: Cardiac remodelling,Background Ca2+ entry,Calcium,Ion channels,TRPC1/TRPC4

Data availability:

Keywords: Cardiac remodelling, Background Ca2+ entry, Calcium, Ion channels, TRPC1/TRPC4

A background Ca2+ entry pathway mediated by TRPC1/TRPC4 is critical for development of pathological cardiac remodelling.

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