Exploring the role of TRPM4 in calcium‐dependent triggered activity and cardiac arrhythmias
Andy Pironet, Frone Vandewiele, Rudi Vennekens
Abstract
Abstract Cardiac arrhythmias pose a major threat to a patient's health, yet prove to be often difficult to predict, prevent and treat. A key mechanism in the occurrence of arrhythmias is disturbed Ca 2+ homeostasis in cardiac muscle cells. As a Ca 2+ ‐activated non‐selective cation channel, TRPM4 has been linked to Ca 2+ ‐induced arrhythmias, potentially contributing to translating an increase in intracellular Ca 2+ concentration into membrane depolarisation and an increase in cellular excitability. Indeed, evidence from genetically modified mice, analysis of mutations in human patients and the identification of a TRPM4 blocking compound that can be applied in vivo further underscore this hypothesis. Here, we provide an overview of these data in the context of our current understanding of Ca 2+ ‐dependent arrhythmias. image