Studies in vivo have demonstrated that knockout mice lacking the TRPV1 gene (TRPV1-/-) exhibit notable enhancements in cardiac function accompanied by reductions in hypertrophy, fibrosis, and apoptosis following TAC, substantiating the role of TRPV1 in the maladaptive remodeling induced by mechanical stress186. This evidence concerns the gene TRPV1 and persistent truncus arteriosus.