2014
DOI: 10.1016/j.ceca.2014.02.019
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TRPM7 is involved in angiotensin II induced cardiac fibrosis development by mediating calcium and magnesium influx

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Cited by 58 publications
(51 citation statements)
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“…One of our previous studies has shown that nifedipine and verapamil, classical blockers of L-type calcium channels, had no effect on angiotensin II-induced elevation of [Ca 2+ ] i in cardiac fibroblasts (33), indicating some channels other than voltage-dependent calcium channels may contribute to the increase of [Ca 2+ ] i in cardiac fibroblasts and resultant fibrosis. Furthermore, our recent studies have demonstrated that TRPM7 is involved in angiotensin II-induced cardiac fibrosis by mediating calcium influx in cardiac fibroblasts (34). These findings indicate that TRPM7-mediated Ca 2+ influx plays a crucial role in myocardial fibrogenesis.…”
Section: +mentioning
confidence: 81%
“…One of our previous studies has shown that nifedipine and verapamil, classical blockers of L-type calcium channels, had no effect on angiotensin II-induced elevation of [Ca 2+ ] i in cardiac fibroblasts (33), indicating some channels other than voltage-dependent calcium channels may contribute to the increase of [Ca 2+ ] i in cardiac fibroblasts and resultant fibrosis. Furthermore, our recent studies have demonstrated that TRPM7 is involved in angiotensin II-induced cardiac fibrosis by mediating calcium influx in cardiac fibroblasts (34). These findings indicate that TRPM7-mediated Ca 2+ influx plays a crucial role in myocardial fibrogenesis.…”
Section: +mentioning
confidence: 81%
“…Firstly, previous studies have shown that TRPM7 vastly accelerated cardiac fibrosis responding to pathological stimulus through Ca 2+ influx [13,45]. And it has been reported that TRPM7 is negatively regulated by intracellular levels of Mg 2+ and Mg-ATP [46], which means that the increased [Mg 2+ ] i is sufficient to inhibit TRPM7 channels.…”
Section: Discussionmentioning
confidence: 99%
“…of cardiac fibroblasts [12]. The early studies in our laboratory have found that stimulation of Ang II in cardiac fibroblasts elicits an extrusion of cellular Mg 2+ [13]. And Ang II is known to activate the Na + /Mg 2+ exchanger in vascular and renal cells to expedite the development of hypertension through enhancing vascular reactivity, vascular remodeling and/or impairing vasodilation [14].…”
Section: Introductionmentioning
confidence: 99%
“…22 TRPM7 protein expression increases by 24 hours in the presence of angiotensin II. 44 Silencing TRPM7 channels by short hairpin RNA interference reduced hydrogen peroxide-induced activation of Ca 2+ influx and 2-aminoethoxydiphenylborate, a TRPM7 blocker that could inhibit hydrogen peroxide-induced cardiac fibrosis. 28 In addition to Ca 2+ , another permeant ion, Mg 2+ --an essential cofactor in numerous enzymatic reactions via Mg 2+ -dependent regulation of MAPK, tyrosine kinases, reactive oxygen species and important signaling molecules --is involved in cell proliferation, differentiation, inflammation, etc.…”
Section: Trpc1 Channelsmentioning
confidence: 99%