Cardiac fibrosis is involved in the occurrence and development of various cardiac diseases, leading to cardiac remodeling, dysfunction, heart failure and even death. The pathological bases of cardiac fibrosis are the proliferation and differentiation of cardiac fibroblasts and the excessive deposition of extracellular matrix. Transient receptor potential (TRP) channels are non-selective cationic channels, regulating cell functions mainly via Ca2+ influx. Increasing studies have shown that TRP channels are involved in the regulation of many physiological functions and the occurrence and development of cardiac fibrosis. This article reviews the mechanism of cardiac fibrosis and TRP channels seen as a new target for its treatment.