Fibroblast and cardiomyocyte specific TREK-1 deficiency in heart failure
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Date
2021-05
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The Ohio State University
Abstract
Cardiac arrhythmias are a major outcome of heart failure that result in sudden cardiac death. While various causes of arrhythmias have been studied, the exact molecular and cellular mechanisms responsible for generating these life-threatening arrhythmias remain unclear. Our lab has previously studied the cardiac two-pore potassium channel, TREK-1, at the cellular level to understand its role in sinoatrial node membrane excitability. In this study, we aim to investigate the precise mechanism of TREK-1 function at the whole heart level through the use of mouse models with cardiomyocyte and cardiac fibroblast-specific TREK-1 deficiency. High resolution optical mapping experiments of ex-vivo hearts were performed to investigate how electrical signals propagate across the heart. Results obtained from this study will help determine the exact arrhythmic mechanisms of TREK-1 in both cardiomyocytes and cardiac fibroblasts.