Cellular Senescence, Insulin Resistance, and CDKN2B: An Intrinsic Connection in Metabolic Diseases

This review summarizes the pivotal roles of insulin resistance (IR) and cellular senescence in metabolic diseases, focusing on how adipocyte and hepatocyte senescence promote IR and the progression of type 2 diabetes through the senescence-associated secretory phenotype (SASP) and key signaling pathways (e.g., p53, Akt/FoxO1). The article further focuses on the cell cycle regulatory gene CDKN2B and its non-coding RNA (CDKN2B-AS), elucidating their expression alterations and genetic susceptibility in various metabolic diseases including atherosclerosis, coronary heart disease, polycystic ovary syndrome, and diabetes. Although the role of CDKN2B in aging and metabolic regulation remains unclear, existing evidence suggests it may exert complex and critical regulatory effects on the pathogenesis of metabolic diseases by influencing insulin resistance patterns and tissue-specific senescence phenotypes. Future research should further elucidate the functional differences of CDKN2B and its isoforms across various tissues and disease states.