Low-dose administration of human recombinant irisin (r-irisin) can reduce myocardial fibrosis and left ventricular function in diabetic mice, while high-dose r-irisin can stimulate mitogen-activated protein kinase (MAPK) signaling, thus upregulating matrix metalloproteinases (MMPs) in response to high-glucose environment, ultimately promoting the proliferation and migration of cardiac fibroblasts, and leading to excessive collagen deposition [27]. The gene discussed is FNDC5; the disease is Myocardial fibrosis.