NFKB1 and Myocardial fibrosis: The combination of AGEs and RAGE induces the production of reactive oxygen species, followed by activation of major cellular signal transduction pathways, such as the NF-κB signaling pathway, resulting in the regulation of a variety of inflammatory and profibrotic factors, such as CD68 and matrix metalloproteinases (MMPs), which cause vascular endothelial damage, cardiomyocyte edema degeneration, myocardial fibrosis and other pathological changes, and are involved in the development of diabetes-induced cardiovascular complications [17–20].