Abstract
Transient receptor potential canonical (TRPC) channels are involved in the regulation of cardiac function under (patho)physiological conditions and are closely associated with the pathogenesis of cardiac hypertrophy, arrhythmias, and myocardial infarction. Understanding the molecular mechanisms and the regulatory pathway/locus of TRPC channels in related heart diseases will provide potential new concepts for designing novel drugs targeting TRPC channels. We will present the properties and regulation of TRPC channels and their roles in the development of various forms of heart disease. This article provides a brief review on the role of TRPC channels in the regulation of myocardial function as well as how TRPC channels may serve as a therapeutic target in heart failure and cardiac arrhythmias including atrial fibrillation.
Highlights
Transient receptor potential (TRP) channels are transmembrane non-selective cation channels
Another piece of evidence has demonstrated that NADPH oxidase 2 (Nox2) serves as a main source of reactive oxygen species (ROS) in cardiomyocytes and is able to form a stable complex with TRPC3 channels, while the TRPC3-Nox2 complex plays an important role in regulating doxorubicin-induced myocardial atrophy [49]
TRPC3 and TRPC6 regulate a Ca2+ signaling pathway mediated by diacylglycerol (DAG), which is crucial in AngII-induced nuclear factor of activated T cells (NFAT) and cardiac hypertrophy [58]
Summary
Transient receptor potential (TRP) channels are transmembrane non-selective cation channels. A large number of recent studies have found that classical transient receptor potential canonical (TRPC) channels are involved in the regulation of cardiac function and are closely related to the pathogenesis of cardiac hypertrophy, fibrosis, arrhythmias, and myocardial infarction. A series of gene knock-out studies found that TRPC1, TRPC3, and TRPC6 are associated with cardiac hypertrophy [4,5,6] and that deletion of or impaired function of TRPC3 leads to cardiac conduction block [7, 8]. The expression and electrical function of TRPC3 and TRPC6 channels have been detected in cardiac fibroblasts and plays a role in cardiac fibrosis resulting in fibrosis-associated heart diseases [10, 11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
