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10.1016/j.ceca.2014.02.019 http://scihub22266oqcxt.onion/10.1016/j.ceca.2014.02.019 24680379!ä!24680379 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Calcium 2014 ; 55 (5): 252-60 Nephropedia Template TP {{tp|p=24680379|t=2014. TRPM7 is involved in angiotensin II induced cardiac fibrosis development by mediating calcium and magnesium influx |pdf=|usr=}}{{24680379}} gab.com Text TRPM7 is involved in angiotensin II induced cardiac fibrosis development by mediating calcium and magnesium influx JO: Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=24680379 #FOAvip 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 Ca(2+) and Mg(2+). 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. Twit Text FOAVip TRPM7 is involved in angiotensin II induced cardiac fibrosis development by mediating calcium and magnesium influx ????Cell Calcium http://www.kidney.de/pget.php?&tw=1&pmid=24680379 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24680379 #FOAvip English Wikipedia <ref>{{Cite pmid|24680379}}</ref> TRPM7 is involved in angiotensin II induced cardiac fibrosis development by mediating calcium and magnesium influx #MMPMID24680379 Yu Y; Chen S; Xiao C; Jia Y; Guo J; Jiang J; Liu P Cell Calcium 2014[May]; 55 (5): 252-60 PMID24680379show ga 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 Ca(2+) and Mg(2+). 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. |Actins/metabolism[MESH] |Angiotensin II/pharmacology[MESH] |Animals[MESH] |Boron Compounds/pharmacology[MESH] |Calcium/*metabolism[MESH] |Cell Proliferation/drug effects[MESH] |Cells, Cultured[MESH] |Connective Tissue Growth Factor/metabolism[MESH] |Cyclin-Dependent Kinase Inhibitor p27/metabolism[MESH] |Down-Regulation/drug effects[MESH] |Fibroblasts/cytology/drug effects/metabolism[MESH] |Fibrosis/chemically induced/metabolism/pathology[MESH] |Magnesium/*metabolism[MESH] |Male[MESH] |NFATC Transcription Factors/metabolism[MESH] |Nerve Tissue Proteins/metabolism[MESH] |RNA Interference[MESH] |RNA, Small Interfering/metabolism[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH]TRPM7 is involved in angiotensin II induced cardiac fibrosis developme(epmc).pdf DeepDyve Pubget Overpricing