Transient receptor potential (TRP) channels are nonselective cationic channels that are generally Ca2+ permeable and have a heterogeneous expression in the heart. In the myocardium, TRP channels participate in several physiological functions, such as modulation of action potential waveform, pacemaking, conduction, inotropy, lusitropy, Ca2+ and Mg2+ handling, store-operated Ca2+ entry, embryonic development, mitochondrial function and adaptive remodelling. Moreover, TRP channels are also involved in various pathological mechanisms, such as arrhythmias, ischaemia–reperfusion injuries, Ca2+-handling defects, fibrosis, maladaptive remodelling, inherited cardiopathies and cell death. In this Review, we present the current knowledge of the roles of TRP channels in different cardiac regions (sinus node, atria, ventricles and Purkinje fibres) and cells types (cardiomyocytes and fibroblasts) and discuss their contribution to pathophysiological mechanisms, which will help to identify the best candidates for new therapeutic targets among the cardiac TRP family.
Transient receptor potential (TRP) channels show heterogeneous expression between cardiac regions (sinus node, atria, Purkinje fibres and ventricles) and cell types (myocytes or fibroblasts).
TRP channels are important in major physiological processes in the heart, such as regulation of Ca2+ homeostasis, contractility, pacemaking, conduction, modulation of the action potential, embryonic development and mitochondrial function.
Cardiac pathologies are often associated with remodelling of TRP channel expression.
TRP channel remodelling participates in the progression of cardiac diseases.
Targeting TRP channels might be an interesting therapeutic strategy for cardiac pathologies.
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L.S. and R.G. are supported by a grant from “Région Normandie”. The authors acknowledge R. Coronel (IHU-Liryc, Bordeaux Université, France, and Academic Medical Center, University of Amsterdam, Netherlands) for helpful advice and R. Walton (IHU-Liryc, Bordeaux Université, France) for English editing of the manuscript.
Nature Reviews Cardiology thanks M. Nishida and the other anonymous reviewer(s) for their contribution to the peer review of this work.