premature ventricular contractions (PVCs) is the most common cardiac arrhythmia in patients, while some of them could develop cardiac dysfunction in the several years. According to different characteristics in patients, risk factors for premature ventricular contraction-induced cardiomyopathy (PVICM) are complex and diverse, including PVC burden, PVC QRS duration PVC origin and sexuality. Investigation of molecular mechanisms has predominantly been studied in animal models, primarily swine and canine. Based on those models, typical tissue alterations in PVICM are mild fibrosis and eccentric hypertrophy. Besides, frequent PVCs enhance sympathetic activity, further exacerbating structural alteration in models. Substructural remodeling includes reduced T-tubules, decreased dyad intensity and Z-line arrangement disarray, leading to reduced L-type calcium currents and decreased systolic calcium transient synchrony. All of the changes might function corporately or separately, resulting in cardiac dysfunction and malignant arrhythmia, increase the risk of sudden cardiac death. PESP, post-extrasystolic potentiation; JPH2, junctophilin-2; BIN1, bridging integrator-1; APD, action potential duration; Ito, transient outward K{}^{+} currents; IK1, inward rectifier K{}^{+} currents; ICaL, L-type Ca{}^{2+} currents. Created with https://biorender.com/.