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Vascular smooth muscle cell senescence in atherosclerosis
Abstract
Markers of cell senescence have been identified in both the blood and vessel wall of patients with atherosclerosis. In particular, vascular smooth muscle cells (VSMCs) derived from human plaques show numerous features of senescence both in culture and in vivo. This review summarises the evidence for VSMC senescence in atherosclerosis, and outlines the mechanisms and triggers leading to their senescence.
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“In addition, senescent endothelial and smooth muscle cells have been implicated in the genesis or promotion of age-related cardiovascular disease (126, 127).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [127]
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“Unstable mature plaques show low VSMC proliferation and clear evidence of VSMC senescence 191 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [191]
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“In addition, senescent endothelial and smooth muscle cells have been implicated in the genesis or promotion of age-related cardiovascular disease (126, 127).”
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“However, unstable mature plaques show low levels of VSMC proliferation and clear evidence of VSMC senescence.(6) Similarly, restenotic neointimas also contain senescent VSMCs.”
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“Different research groups have shown that VSMC senescence is present in atherosclerotic plaques and contributes to the pathogenesis of atherosclerosis.(21,32,53,54) Our observations confirm once more the dual role of VSMCs in atherosclerosis.”
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“Senescent VSMCs are associated with oxidative DNA damage, impaired DNA repair, and telomere shortening (74, 75).”
BackgroundLin, C., Tang, X., Zhu, Z., Liao, X., Zhao, R., Fu, W., Chen, B., Jiang, J., Qian, R., & Guo, D. (2014) · Lipids in Health and Disease · doi:10.1186/1476-511x-13-14 · Cited by 58
“It was observed that human plaque–derived VSMCs illustrated numerous features of senescence [21]: (1) restricted proliferative capacity, (2) high senescenceassociated β-galactosidase (SAβG) activity even at early stages of culture, (3) significantly reduced percentage of S phase cells and increased percentage of cells…”
BackgroundTargeting normal and cancer senescent cells as a strategy of senotherapy
Sikora, E., Bielak-Żmijewska, A., & Mosieniak, G. (2019) · Ageing Research Reviews · doi:10.1016/j.arr.2019.100941 · Cited by 59
Neuregulin-1, a potential therapeutic target for cardiac repair
Wang, Y., Wei, J.-L., Zhang, P., Zhang, X., Wang, Y., Chen, W., Zhao, Y., & Cui, X. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.945206 · Cited by 58
“Oxidative stress and hyperglycemia are the two main factors that contribute to SIPS (Gorenne et al., 2006; Minamino and Komuro, 2007; Sikora et al., 2011).”
BackgroundInfluentialHistone deacetylases and atherosclerosis
Zheng, X., Zhou, T., Wang, X., Tong, X.-H., & Ding, J. (2014) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2014.12.048 · Cited by 56
Zhou, T., Zhang, M., Zhao, L., Li, A., & Qin, X. (2016) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00093.2016 · Cited by 54
“It has been hypothesized that VSMC senescence promotes the thinning of fibrous caps and the instability of atherosclerotic plaques (16).”
BackgroundSenescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer
Banerjee, P., Kotla, S., Velatooru, L. R., Abe, R. J., Olmsted‐Davis, E. A., Cooke, J. P., Schadler, K., Deswal, A. M., Herrmann, J., Lin, S. H., et al. (2021) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2021.763930 · Cited by 54
Ahmad, F., & Leake, D. S. (2018) · Journal of Lipid Research · doi:10.1194/jlr.m088245 · Cited by 55
“Not only is cellular senescence associated with atherosclerosis, there is growing evidence that cellular senescence may promote atherosclerosis (32-34).”
BackgroundLi, Y., Qin, R., Yan, H., Wang, F., Huang, S., Zhang, Y., Zhong, M., Zhang, W., & Wang, Z. (2017) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2017.09.012 · Cited by 55
Głuchowska, A., Cysewski, D., Baj‐Krzyworzeka, M., Szatanek, R., Węglarczyk, K., Podszywalow‐Bartnicka, P., Sunderland, P., Kozłowska, E., Śliwińska, M. A., Dąbrowski, M., et al. (2022) · GeroScience · doi:10.1007/s11357-022-00625-0 · Cited by 56
“Accumulation of senescent VSMCs within the area of plaque formation promotes its instability due to lack of proliferation and impaired production of extracellular matrix, both leading to the weak-ening of the fibrous cap [4].”
Slowing Down Ageing: The Role of Nutrients and Microbiota in Modulation of the Epigenome
Gadecka, A., & Bielak-Żmijewska, A. (2019) · Nutrients · doi:10.3390/nu11061251 · Cited by 56
NOX4 downregulation leads to senescence of human vascular smooth muscle cells
Przybylska, D., Janiszewska, D., Goździk, A., Bielak-Żmijewska, A., Sunderland, P., Sikora, E., & Mosieniak, G. (2016) · Oncotarget · doi:10.18632/oncotarget.12079 · Cited by 52
“Moreover, growth arrested VSMCs significantly restrict the repair capacity of the plaque, which contributes to high risk of myocardial infarction and stroke [32, 33, 34].”
Nalapareddy, K., Jiang, H., Gutierrez, L. M. G., & Rudolph, K. L. (2008) · Experimental Gerontology · doi:10.1016/j.exger.2008.09.002 · Cited by 50
“…keratinocytes (Dimri et al., 1995), cornea epithelium (Mimura and Joyce, 2006), ischemic heart (Minamino et al., 2002), arteriosclerotic plaques (Gorenne et al., 2006), articular chondrocytes (Martin and Buckwalter, 2001), and in liver cirrhosis – the end stage of chronic liver disease (Wiemann…”
BackgroundInfluentialDPP4 inhibition impairs senohemostasis to improve plaque stability in atherosclerotic mice
Herman, A. B., Tsitsipatis, D., Anerillas, C., Mazan-Mamczarz, K., Carr, A. E., Gregg, J. M., Wang, M., Zhang, J., Michel, M., Henry-Smith, C. A., et al. (2023) · Journal of Clinical Investigation · doi:10.1172/jci165933 · Cited by 50
“Given that DPP4 levels and activity increase with hVSMC senescence, we asked whether DPP4 is elevated in atherosclerosis, a disease in which senescent VSMCs have been implicated (24).”
Molecular mechanisms and cardiovascular implications of cancer therapy-induced senescence
Abdelgawad, I. Y., Sadak, K. T., Lone, D. W., Dabour, M. S., Niedernhofer, L. J., & Zordoky, B. N. M. (2020) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2020.107751 · Cited by 47
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Wang, X., Zhu, L., Liu, J., Ma, Y., Qiu, C., Liu, C., Gong, Y., Yuwen, Y., Guan, G., Zhang, Y., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-45582-8 · Cited by 45
“The clinical implications of this molecular cascade could be foreseen, as the HES1/SIRT1/P21 axis is central to VSMC senescence, a factor in atherosclerotic progression and plaque instability 32 .”
HDL slowing down endothelial progenitor cells senescence: A novel anti-atherogenic property of HDL
Pu, D., & Liu, L. (2007) · Medical Hypotheses · doi:10.1016/j.mehy.2007.05.025 · Cited by 44
Anthracycline chemotherapy‐mediated vascular dysfunction as a model of accelerated vascular aging
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Böhm, A., Flößer, A., Ermler, S., Fender, A. C., Lüth, A., Kleuser, B., Schrör, K., & Rauch, B. H. (2013) · Cardiovascular Research · doi:10.1093/cvr/cvt112 · Cited by 42
“It should be noted that cultured SMC do not necessarily behave in a manner similar to SMC in atherosclerotic lesions and also divergent SMC subtypes within atherosclerotic plaques have been described.(34,35) Thus, further mechanistic studies may address the functional interaction of FXa effects and the S1P pathway in…”
ResultThe Senolytic Drug JQ1 Removes Senescent Cells via Ferroptosis
Go, S., Kang, M., Kwon, S. P., Jung, M., Jeon, O. H., & Kim, B. (2021) · Tissue Engineering and Regenerative Medicine · doi:10.1007/s13770-021-00346-z · Cited by 42
“Cellular senescence is one of the hallmarks of aging [15], and the accumulation of senescent cells in tissues is affected in many age-related degenerative diseases, including tumors, arthritis [16], Alzheimer’s disease [17], diabetes [18], heart diseases [19, 20], atherosclerosis [21], and various other conditions [22…”
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“Further studies will be required to assess how early modification in the plaques of mice exposed to (137)Cs may alter lesion composition at later time points, with special consideration for smooth muscle cell content (since VSMCs are the main cell type responsible for collagen synthesis in the plaque [8]) and inflamma…”
BackgroundPharmacological aspects of fisetin
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“in the development of restenosis after percutaneous coronary intervention as well as in the pathogenesis of hypertension and the progression of atherosclerosis).([1,2]) Reactive oxygen species (ROS) are involved in many pathophysiological processes of VSMCs, such as growth, migration, contraction and differentiation.”
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“Short telomeres have been implicated in vascular senescence and atherosclerosis [111].”
BackgroundHistone Deacetylase SIRT1, Smooth Muscle Cell Function, and Vascular Diseases
Wang, F., & Chen, H. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.537519 · Cited by 40
Peroxisome proliferator-activated receptor delta and cardiovascular disease
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Gadecka, A., Nowak, N., Bulanda, E., Janiszewska, D., Dudkowska, M., Sikora, E., & Bielak-Żmijewska, A. (2025) · GeroScience · doi:10.1007/s11357-024-01504-6 · Cited by 39
“This cell type is directly involved in the development and progression of atherosclerosis and cardiovascular problems [15].”
Metadata
- Authors
- GORENNE, I., KAVURMA, M., SCOTT, S., & BENNETT, M.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- BENNETT, M
- ORCID
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-10-01
- Volume
- 72
- Issue
- 1
- Pages
- 9-17
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2155554546
- Cited by
- 196
- References
- 108
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 11 · 2023: 7 · 2022: 14 · 2021: 15 · 2020: 13 · 2019: 14 · 2018: 9 · 2017: 16 · 2016: 11 · 2015: 12 · 2014: 11 · 2013: 12 · 2012: 8
- FWCI
- 0.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- vascular smooth muscle cells, cellular senescence, atherosclerosis, atherosclerotic plaque, senescence markers, senescence mechanisms, plaque macrophages
- MeSH terms
- beta-Galactosidase, Cell Cycle, Humans, Muscle, Smooth, Vascular, Telomere, Cellular Senescence, Cell Proliferation, Atherosclerosis
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