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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.