Cited by 133Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsSirtuins and Resveratrol in Medicine

Role of Cellular Senescence in Type II Diabetes

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Narasimhan, Akilavalli, Flores, Rafael R, Robbins, Paul D, Niedernhofer, Laura J·2021·Endocrinology

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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  • Senescent cell clearance improves glucose homeostasis and insulin sensitivity in obese and aged mice.

    “Senescent cell clearance improved glucose homeostasis and insulin sensitivity in obese and aged mice103.”

    From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [103]

    The Adipose Tissue Senescence and Inflammation section reports that senolytics significantly improve glucose tolerance and insulin sensitivity in mice on a high-fat diet, supporting the claim for obese mice. The copy does not report those improvements following senescent-cell clearance in aged mice; its discussion of old mice concerns senescence markers and insulin resistance. Page numbers are unavailable in the indexed passages. (LLM, conf=0.88)

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Research works printed but not linked: 3

  1. [48]48. Ressler S, Bartkova J, Niederegger H, et al. p16INK4A is a ro- bust in vivo biomarker of cellular aging in human skin. Aging Cell. 2006;5(5):379-389.
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Authors
Narasimhan, A., Flores, R. R., Robbins, P. D., & Niedernhofer, L. J.
Affiliations
University of Minnesota (US)
Corresponding author
Niedernhofer, Laura J
Venue
Endocrinology
Published
2021-08-07
Volume
162
Issue
10
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
OpenAlex
W3188031952
Cited by
133
References
151
Citations by year
2026: 21 · 2025: 39 · 2024: 36 · 2023: 21 · 2022: 12 · 2021: 3
FWCI
2.40
Type
journal article
Language
en
Open access
Locations
  • Endocrinology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (P01 R01 AG063543, R01 AG043376, U19 AG056278, P01 AG062413)
  • National Institute on Aging
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
Keywords
cellular senescence, type 2 diabetes, senescence-associated secretory phenotype, beta-cell dysfunction, insulin resistance, adipose tissue dysfunction, aging, obesity, hyperglycemia, diabetes complications, inflammation
MeSH terms
Senescence-Associated Secretory Phenotype, Adipose Tissue, Aging, Animals, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Diabetic Retinopathy, Disease Models, Animal, Humans, Hyperglycemia, Immune System, Inflammation, Insulin, Insulin Resistance, Obesity, Phenotype, Cellular Senescence, Insulin-Secreting Cells, Mice, TOR Serine-Threonine Kinases

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