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2型糖尿病是一种与年龄密切相关的疾病,随着年龄增加,胰岛β细胞增殖能力和分泌能力下降,糖尿病患病率明显增加,但其机制尚不清楚.最近研究发现,细胞周期蛋白依赖激酶(cyclin-dependent kinase,CDK)抑制剂p16INK4a是引起胰岛β细胞年龄相关性老化的重要调控因子.研究表明,通过p16INK4a介导的胰岛老化机制可能有如下两个:p38MAPK(mitogen-activated proteinkinase)途径和PDGFR(platelet-derived growth factor receptor)途径,两者均引起p16ink4a及p19ARF表达增加,而损害胰岛细胞增殖.本文综述年龄相关性胰岛β细胞功能下降的潜在机制,从而为改善胰岛β细胞功能提供新的分子靶点.
Type 2 diabetes is an age-related disease, with increasing age, pancreatic β-cell proliferation and secretion decreased, the prevalence of diabetes increased significantly, but the mechanism is unclear.Recently found that cyclin dependent P16INK4a, a cyclin-dependent kinase (CDK) inhibitor, is one of the important regulators of age-related aging of pancreatic islet β cells.It is suggested that p16INK4a may play an important role in the pathogenesis of islet aging as follows: p38MAPK (mitogen-activated proteinkinase) Pathways and platelet-derived growth factor receptor (PDGFR) pathways, both of which cause the expression of p16ink4a and p19ARF to increase, and impair the proliferation of islet cells.This paper reviews the potential mechanism of age-related decline of islet β-cell function, Provide new molecular targets.