The DOI matches its Crossref record; 179 of the 181 references it cites were found in a registry or an index.
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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“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]
In the citing paper
“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]
In the citing paper
“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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Cites
1 retracted
Myocyte Turnover in the Aging Human Heart
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BackgroundBone marrow cells regenerate infarcted myocardium
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BackgroundMethodSelf-citationAdult Cardiac Stem Cells Are Multipotent and Support Myocardial Regeneration
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Research works printed but not linked: 2
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Ferrucci, L., Gonzalez‐Freire, M., Fabbri, E., Simonsick, E., Tanaka, T., Moore, Z., Salimi, S., Sierra, F., & de Cabo, R. (2020) · Aging Cell · doi:10.1111/acel.13080 · Cited by 781
Mechanisms and consequences of endothelial cell senescence
Bloom, S. I., Islam, M. T., Lesniewski, L. A., & Donato, A. J. (2022) · Nature Reviews Cardiology · doi:10.1038/s41569-022-00739-0 · Cited by 521
Cai, Y., Song, W., Li, J., Jing, Y., Liang, C., Zhang, L., Zhang, X., Zhang, W., Liu, B., An, Y., et al. (2022) · Science China Life Sciences · doi:10.1007/s11427-022-2161-3 · Cited by 450
Gut microbiota and cardiovascular disease: opportunities and challenges
Kazemian, N., Mahmoudi, M., Halperin, F. A., Wu, J. C., & Pakpour, S. (2020) · Microbiome · doi:10.1186/s40168-020-00821-0 · Cited by 404
Ferrucci, L., Levine, M. E., Kuo, P.-L., & Simonsick, E. M. (2018) · Circulation Research · doi:10.1161/circresaha.118.312816 · Cited by 303
Metadata
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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