MAPK14 and Hyperglycemia: Sustained hyperglycemia, however, would induce β cell senescence via multiple possible mechanisms, such as apoptosis signaling-regulating kinase 1 activation [30], p38 mitogen-activated protein kinase activation [31], and “glycolytic overload” (characterized by the increased metabolic flux through glycolysis in hyperglycemia and the decreased proteolysis of hexokinase) mediated mitochondrial dysfunction [32].