Institute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, 55455, USA.
Endocrinology. 2021 Oct 1;162(10). doi: 10.1210/endocr/bqab136.
Cellular senescence is a cell fate that occurs in response to numerous types of stress and can promote tissue repair or drive inflammation and disruption of tissue homeostasis depending on the context. Aging and obesity lead to an increase in the senescent cell burden in multiple organs. Senescent cells release a myriad of senescence-associated secretory phenotype factors that directly mediate pancreatic β-cell dysfunction, adipose tissue dysfunction, and insulin resistance in peripheral tissues, which promote the onset of type II diabetes mellitus. In addition, hyperglycemia and metabolic changes seen in diabetes promote cellular senescence. Diabetes-induced cellular senescence contributes to various diabetic complications. Thus, type II diabetes is both a cause and consequence of cellular senescence. This review summarizes recent studies on the link between aging, obesity, and diabetes, focusing on the role of cellular senescence in disease processes.
细胞衰老(Cellular senescence)是一种细胞命运,它会对多种类型的应激做出反应,并且可以根据具体情况促进组织修复或引发炎症和组织稳态的破坏。衰老和肥胖会导致多个器官中衰老细胞负担的增加。衰老细胞会释放出大量与衰老相关的分泌表型因子,这些因子直接介导胰腺β细胞功能障碍、脂肪组织功能障碍和外周组织的胰岛素抵抗,从而促进 II 型糖尿病的发生。此外,糖尿病患者中出现的高血糖和代谢变化会促进细胞衰老。糖尿病引起的细胞衰老会导致各种糖尿病并发症。因此,II 型糖尿病既是细胞衰老的原因也是结果。这篇综述总结了最近关于衰老、肥胖和糖尿病之间联系的研究,重点介绍了细胞衰老在疾病过程中的作用。