In addition, PGF2α/FP receptor activation facilitates the pathogenesis of myocardial fibrosis in individuals with diabetic cardiomyopathy, accompanied by elevated cholesterol, triglyceride, glucose, and insulin levels, increased collagen deposition, and severe insulin resistance by activating PKC/Rho pathways, while FP receptor gene silencing alleviates myocardial fibrosis mainly by inhibiting this process [94,95]. This evidence concerns the gene INS and diabetic cardiomyopathy.