MAPK14 and Hyperglycemia: From the mechanism perspective, beta cell function dysfunction leads to hyperglycemic and hypoinsulinemic states, and it was demonstrated that hyperglycemia promotes proliferation and activation of pancreatic stellate cells (PSCs) and stimulates collagen production of PSCs via the protein kina-seC-p38 mitogen-activated protein kinase pathway, resulting in pancreatic fibrosis [40], while hypoinsulinemia inhibits acinar cell growth and synthesis of pancreatic enzymes [41].