Cited by 134Telomeres, Telomerase, and SenescenceSirtuins and Resveratrol in MedicineGenetics, Aging, and Longevity in Model Organisms

Cellular senescence links aging and diabetes in cardiovascular disease

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Shakeri, Hadis, Lemmens, Katrien, Gevaert, Andreas B., De Meyer, Guido R. Y., Segers, Vincent F. M.·2018·American Journal of Physiology-Heart and Circulatory Physiology

Abstract

Aging is a powerful independent risk factor for cardiovascular diseases such as atherosclerosis and heart failure. Concomitant diabetes mellitus strongly reinforces this effect of aging on cardiovascular disease. Cellular senescence is a fundamental mechanism of aging and appears to play a crucial role in the onset and prognosis of cardiovascular disease in the context of both aging and diabetes. Senescent cells are in a state of cell cycle arrest but remain metabolically active by secreting inflammatory factors. This senescence-associated secretory phenotype is a trigger of chronic inflammation, oxidative stress, and decreased nitric oxide bioavailability. A complex interplay between these three mechanisms results in age- and diabetes-associated cardiovascular damage. In this review, we summarize current knowledge on cellular senescence and its secretory phenotype, which might be the missing link between aging and diabetes contributing to cardiovascular disease.

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Crossref · 10.1152/ajpheart.00287.2018

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  • Persisting senescent cells have been tied to multiple chronic diseases other than atherosclerosis.

    “These persisting senescent cells have been recently tied to multiple chronic diseases other than atherosclerosis, including diabetes mellitus,85 obesity,85 Alzheimer’s disease,86 heart failure,10,87 idiopathic pulmonary fibrosis,88,89 chronic obstructive pulmonary disease,90 chronic kidney disease,91 cancer,92 and osteoarthritis.93”

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  1. [24]24. Chen J, Huang X, Halicka D, Brodsky S, Avram A, Eskander J, Bloomgarden NA, Darzynkiewicz Z, Goligorsky MS. Contribution of p16INK4a and p21CIP1 pathways to induction of premature senescence of human endothelial cells: permissive role of p53. Am J Physiol Heart - Circ Physiol 290: H1575-H1586, 2006. doi:10.1152/ajpheart.00364. 2005. · DOI

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Authors
Shakeri, H., Lemmens, K., Gevaert, A. B., De Meyer, G. R. Y., & Segers, V. F. M.
Affiliations
  • University of Antwerp (BE)
  • Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Corresponding author
Segers, Vincent F. M.
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Published
2018-09-01
Volume
315
Issue
3
Pages
H448-H462
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
OpenAlex
W2802682414
Cited by
134
References
204
Citations by year
2026: 17 · 2025: 20 · 2024: 23 · 2023: 16 · 2022: 16 · 2021: 16 · 2020: 9 · 2019: 9 · 2018: 7
FWCI
1.35
Type
journal article
Language
en
Open access
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion, other-oa)
Funders
  • University of Antwerp (IOF-SBO)
  • FWO (1.5.011.18N)
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
cellular senescence, aging, diabetes mellitus, cardiovascular disease, senescence-associated secretory phenotype, chronic inflammation, oxidative stress, nitric oxide bioavailability, atherosclerosis, heart failure, cell cycle arrest
MeSH terms
Aging, Animals, Cardiovascular Diseases, Diabetes Mellitus, Humans, Cellular Senescence

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