Fibrosis is a pathological process characterized by an increase in fibrous connective tissue and a decrease in parenchymal cells within organ tissues. During the progress, it can lead to structural damage and functional decline of the organ. In recent years, research found that non selective cation channel - transient receptor potential vanillin subfamily 1 (TRPV1) is closely related to fibrosis. When this channel is activated, it can increase intracellular cation concentration and cause corresponding physiological and pathological changes, particularly playing a crucial role in regulating tissue fibrosis. In order to further investigate the mechanism of TRPV1 channel inducing organs fibrosis, animal models have become an important tool for relative study. This article will review the role of TRPV1 channels in fibrosis of organs such as the heart, kidney, and pancreas in mice, and summarize the relevant signaling pathways in which TRPV1 channels participate in regulating fibrosis, to provide new ideas for studying the pathogenesis of fibrosis and the development of targeted drugs.