4.5 Review

Role of Cellular Senescence in Type II Diabetes

Journal

ENDOCRINOLOGY
Volume 162, Issue 10, Pages -

Publisher

ENDOCRINE SOC
DOI: 10.1210/endocr/bqab136

Keywords

Diabetes; cellular senescence; aging; obesity; senotherapeutics; inflammation

Funding

  1. NIH/NIA [P01 R01 AG063543, R01 AG043376, U19 AG056278, P01 AG062413]

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Cellular senescence is a cell fate that can either promote tissue repair or drive inflammation, depending on the context. Aging and obesity increase the burden of senescent cells in multiple organs, leading to various diabetic complications.
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 beta-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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