AUTHOR=Ezeani Martin TITLE=TRP Channels Mediated Pathological Ca2+-Handling and Spontaneous Ectopy JOURNAL=Frontiers in Cardiovascular Medicine VOLUME=6 YEAR=2019 URL=https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2019.00083 DOI=10.3389/fcvm.2019.00083 ISSN=2297-055X ABSTRACT=

Ion channel biology offers great opportunity in identifying and learning about cardiac pathophysiology mechanisms. The discovery of transient receptor potential (TRP) channels is an add-on to the opportunity. Interacting with numerous signaling pathways, being activated multimodally, and having prescribed signatures underlining acute hemodynamic control and cardiac remodeling, TRP channels regulate cardiac pathophysiology. Impaired Ca²⁺-handling cause contractile abnormality. Modulation of intracellular Ca²⁺ concentration ([Ca²⁺]_i) is a major part of Ca²⁺-handling processes in cardiac pathophysiology. TRP channels including TRPM4 regulate [Ca²⁺]_i, Ca²⁺-handling and cardiac contractility. The channels modulate flux of divalent cations, such as Ca²⁺ during Ca²⁺-handling and cardiac contractility. Seminal works implicate TRPM4 and TRPC families in intracellular Ca²⁺ homeostasis. Defective Ca²⁺-homeostasis through TRP channels interaction with Ca²⁺-dependent regulatory proteins such as sodium calcium exchanger (NCX) results in abnormal Ca²⁺ handling, contractile dysfunction and in spontaneous ectopy. This review provides insight into TRP channels mediated pathological Ca²⁺-handling and spontaneous ectopy.