Senescent cells: a therapeutic target for cardiovascular disease
Open accessAbstract
Cellular senescence, a major tumor-suppressive cell fate, has emerged from humble beginnings as an in vitro phenomenon into recognition as a fundamental mechanism of aging. In the process, senescent cells have attracted attention as a therapeutic target for age-related diseases, including cardiovascular disease (CVD), the leading cause of morbidity and mortality in the elderly. Given the aging global population and the inadequacy of current medical management, attenuating the health care burden of CVD would be transformative to clinical practice. Here, we review the evidence that cellular senescence drives CVD in a bimodal fashion by both priming the aged cardiovascular system for disease and driving established disease forward. Hence, the growing field of senotherapy (neutralizing senescent cells for therapeutic benefit) is poised to contribute to both prevention and treatment of CVD.
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The SASP is a protracted and chronic source of inflammatory and other plaque-destabilizing factors, gradually contributing to atherosclerosis pathogenesis.
“Emerging experimental evidence indicates that, in contrast to an acute inflammatory response, the SASP is a protracted and chronic source of inflammatory and other plaque-destabilizing factors,9,10 gradually contributing to atherosclerosis pathogenesis.”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [10]
Cellular senescence is accompanied by a pro-inflammatory phenotype known as the senescence-associated secretory phenotype (SASP), which produces pro-inflammatory cytokines, metalloproteinases, and other factors.
“Cellular senescence is defined as an irreversible cell cycle arrest (mechanism outlined in Figure 1)8 and is accompanied by a pro-inflammatory phenotype. The phenotype is referred to as the senescence-associated secretory phenotype (SASP), producing pro-inflammatory cytokines [interleukin (IL)-1α, IL-1β, IL-6, IL-8, IL-18, CCL-2, tumour necrosis factor α (TNF-α)], metalloproteinases (MMP-1, -2, -3”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [10]
Senescent endothelial cells in atherosclerotic plaques secrete VCAM-1 to recruit and differentiate monocytes into foam cell macrophages.
“Importantly, a fraction of dysfunctional endothelial cells in atherosclerotic plaques is senescent (Minamino et al, 2002) and secretes vascular cell adhesion molecule 1 (VCAM‐1) to recruit and differentiate monocytes into foam cell macrophages (Davignon & Ganz, 2004; Childs et al, 2018).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Childs et al, 2018
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- Authors
- Childs, B. G., Li, H., & van Deursen, J. M.
- Affiliations
- Mayo Clinic (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2018-04-02
- Volume
- 128
- Issue
- 4
- Pages
- 1217-1228
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC5873883
- OpenAlex
- W2795134170
- Cited by
- 192
- References
- 181
- Citations by year
- 2026: 17 · 2025: 21 · 2024: 13 · 2023: 24 · 2022: 32 · 2021: 35 · 2020: 27 · 2019: 16 · 2018: 7
- FWCI
- 2.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion, other-oa)
- Funders
- Glenn Foundation for Medical Research
- Fondation pour la Recherche Médicale
- National Institutes of Health
- National Institute on Aging (R01AG057493, T32AG049672)
- National Cancer Institute (R01CA126828, R01CA096985)
- 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 › Genetics › Mesenchymal stem cell research
- Keywords
- cellular senescence, senolytics, senotherapy, cardiovascular disease, aging, age-related diseases, senolytic therapy, cardiovascular aging
- MeSH terms
- Aged, Aging, Animals, Cardiovascular Diseases, Cardiovascular System, Humans, Cellular Senescence
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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