Cav1, encoding caveolin-1, is a major protein of plasma membrane microdomains called caveolae. It is involved in several signaling pathways and located at the adipocyte lipid droplet [5]. Caveolin-1 has been shown to influence tumorigenicity, with its polymorphisms potentially related to cancer risks. It also plays roles in cell senescence, immune microenvironment regulation, and fibrosis-related processes [6,7,8]. Genetic models can help understand the functions of Cav1 and its polymorphisms in these biological processes.

In cancer-related studies, certain Cav1 polymorphisms such as rs1049334 are associated with an increased risk of urinary cancer, while rs1049337 and rs7804372 may act as protectors [1]. In breast cancer, rs3807987 and rs7804372 polymorphisms are related to the change of breast cancer risk [2]. In prostate cancer, Cav1 is highly expressed, and higher expression is associated with a worse prognosis [3]. In esophageal cancer, down-regulated Cav1 expression is related to a higher tumor mutation burden and a higher rate of response to immune checkpoint inhibitors [7]. In addition, Cav1 promotes epithelial-to-mesenchymal transition (EMT) and chronic renal allograft interstitial fibrosis by activating the ferroptosis pathway, which is important in chronic allograft dysfunction [4]. In atrial fibrillation, Cav1 is critical for the MG53 regulation of TGF-β1 signaling pathway-induced atrial fibrosis [8].

In conclusion, Cav1 is a crucial protein involved in multiple biological processes and diseases. Studies on Cav1, especially those using genetic models, have revealed its significant roles in cancer, fibrosis-related diseases, and other conditions. Understanding Cav1's functions provides insights into disease mechanisms and potential therapeutic targets.