Fibrosis is a pathological process characterized by an increase in connective tissue and a decrease in parenchymal cells within organ tissues. During its progression, fibrosis can lead to structural damage and functional decline of the affected organ. In recent years, it has found that non-selective cation channel transient receptor potential vanilloid subfamily 1 (TRPV1) channel is closely related to fibrosis. When this channel is activated, it can increase the intracellular cation concentration and cause corresponding physiological and pathological changes, playing a particularly crucial role in regulating tissue fibrosis. Animal models have become important tools in studies into the mechanism by which the TRPV1 channel induces organ fibrosis. This article reviews the role of TRPV1 channels in the fibrosis of organs such as the heart, kidney, and pancreas in mice. The relevant signaling pathways in which TRPV1 channels participate to regulate fibrosis are summarized to provide new ideas for studying the pathogenesis of fibrosis and the development of targeted drugs.