Journal
CELL CALCIUM
Volume 55, Issue 5, Pages 252-260Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2014.02.019
Keywords
Cardiac fibrosis; TRPM7; Calcium; Magnesium
Categories
Funding
- National Natural Science Foundation of China [30670837, 81072641, 81273499]
- NSFC-CIHR Joint Health Research Programs [30811120434]
- National Science and Technology Major Project of China Key New Drug Creation and Manufacturing Program [2011ZX09401-307]
- Team Item of Natural Science Foundation of Guangdong Province [S2011030003190]
- Major Project of Guangdong Province [2008A030201013, 2012A080201007]
- Major Project of Guangzhou City [2008Z1-E571]
- Major Project of Department of Education of Guangdong Province [CXZD1006]
- Natural Science Foundation of Guangdong Province [S2012040006327]
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Cardiac fibrosis is involved in a lot of cardiovascular pathological processes. Cardiac fibrosis can block conduction, cause hypoxia, strengthen myocardial stiffness, create electrical heterogeneity, and hamper systolic ejection, which is associated with the development of arrhythmia, heart failure and sudden cardiac death. Besides the initial stimulating factors, the cardiac fibroblasts (CFs) are the principal responsible cells in the fibrogenesis cascade of events. TRPM7, a member of the TRPM (Melastatin) subfamily, is a non-selective cation channel, which permeates both Ca2+ and Mg2+. Here we demonstrated TRPM7 expression in CFs, and 2-APB (TRPM7 inhibitor), inhibited Ang II-induced CTGF, alpha-SMA expression and CFs proliferation. Besides, knocking down TRPM7 by shRNA, we proved that TRPM7 mediated both calcium and magnesium changes in cardiac fibroblasts which contribute to fibrosis progress. This study suggested that TRPM7 should play a pivotal role in cardiac fibroblast functions associated to cardiac fibrosis development. Crown Copyright (C) 2014 Published by Elsevier Ltd. All rights reserved.
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