Abstract
The protein Rad interacts with the LTCC to modulate trigger Ca2+, hence to govern contractility. Reducing Rad levels increases cardiac output. Ablation of Rad also attenuated the inflammatory response following acute myocardial infarction (AMI). Future studies to target deletion of Rad in the heart could be conducted to establish a novel treatment paradigm whereby pathologically stressed hearts would be given a safe, stable positive inotropic support without arrhythmias and without pathological structural remodeling. Future investigations will also focus on establishing inhibitors of Rad, and testing the efficacy of Rad-deletion in cardioprotection relative to the time of onset of AMI.
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