Canonical transient receptor potential 3 channels in atrial fibrillation

European Journal of Pharmacology
Lu Han, Juxiang Li

Abstract

The pathogenesis of atrial fibrillation (AF) is largely dependent on structural remodeling and electrical reconfiguration, which in turn drive localized fibrosis. Canonical transient receptor potential 3 (TRPC3) channel is indispensable regulator of fibrosis development, promoting fibroblasts to transition into myofibroblasts via intracellular Ca2+ overload. TRPC3 is a non-voltage gated, non-selective cation channel that regulates the permeability of the cell to Ca2+. When subjected to various external physical and chemical stimuli, such as angiotensin II (AngII), mechanical stretch, hypoxia, or oxidative stress, TRPC3 coordinates with downstream signal transduction pathways to alter gene expression and thereby regulate a number of distinct pathological patterns and mechanisms. This review will focus on how TRPC3 affects AF pathogenesis by exploring the underlying mechanisms governing fibrosis associated with particular signaling proteins, ultimately highlighting the characteristics of TPRC3 that mark it as a novel therapeutic target for AF alleviation.

Citations

Jan 18, 2020·Cells·Nicole Urban, Michael Schaefer
Nov 17, 2020·International Heart Journal·Jiali XuPinfang Kang
Feb 1, 2020·Pharmacology & Therapeutics·Hongbo WangMichael X Zhu
May 12, 2021·Journal of Molecular and Cellular Cardiology·Dorothee JakobRémi Peyronnet
Jul 25, 2021·International Journal of Molecular Sciences·Natthaphat Siri-AngkulJudith K Gwathmey

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