The transient receptor potential channels (TRP) play important roles under various physiological/pathological conditions. In the heart, several members of TRPC channel subfamily have been demonstrated to play a role in hypertrophy and heart failure. In the TRPM subfamily, TRPM7, TRPM4, and TRPM2 have been shown to be functionally expressed in the heart. Patients carrying TRPM4 mutations develop A-V block. We have demonstrated previously that TRPM7 mediated Ca2+ plays an important role in fibrogenesis and human atrial fibrillation. Here we show that in transverse aortic constriction (TAC) induced hypertrophy and heart failure mouse model, TRPM7 is highly up-regulated. Deletion of Trpm7 significantly increases heart performance in comparison with the wild type (WT) mice after TAC. The ejection fraction is significantly larger and the ratio of heart versus body weight is much smaller in TRPM7-KO mice compared to WT mice after TAC. Moreover, depletion of Trpm7 significantly decreases collagen production and fibrosis formation in TAC induced heart failure mice. Taken together, deletion of Trpm7 can protect against TAC induced heart failure.
37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, SA11
Research Symposium: Physiological functions of melastatin TRPs in the heart
Z. Yue1, J. Xie1, X. Qin1, B. Sun1, Y. Zhang1, J. Du1, B. Liang1, L. Yue1
1. Cardiology/Cell Biology, University of Connecticut Health Center, Farmington, Connecticut, United States.
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