衰老
糖尿病
内分泌学
胰岛素抵抗
背景(考古学)
脂肪组织
内科学
生物
炎症
胰岛素
平衡
细胞生物学
2型糖尿病
医学
免疫学
古生物学
作者
Akilavalli Narasimhan,Rafael R. Flores,Paul D. Robbins,Laura J. Niedernhofer
出处
期刊:Endocrinology
[The Endocrine Society]
日期:2021-08-07
卷期号:162 (10)
被引量:31
标识
DOI:10.1210/endocr/bqab136
摘要
Abstract 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.
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