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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.
Original language | English (US) |
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Pages (from-to) | 1-12 |
Number of pages | 12 |
Journal | Endocrinology (United States) |
Volume | 162 |
Issue number | 10 |
DOIs | |
State | Published - Oct 1 2021 |
Bibliographical note
Funding Information:This work was supported by the NIH/NIA grants P01 R01 AG063543, R01 AG043376, U19 AG056278, and P01 AG062413.
Publisher Copyright:
© The Author(s) 2021.
Keywords
- Aging
- Cellular senescence
- Diabetes
- Inflammation
- Obesity
- Senotherapeutics
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Immune cells as a driver of cell non-autonomous aging
Niedernhofer, L. J. (PI), Arriaga, E. (CoI), Robbins, P. D. (CoI) & Stromnes, I. M. (CoI)
NIH NAT'L INSTITUTE ON AGING (NIA)
4/1/19 → 1/31/24
Project: Research project