Cited by 625Atherosclerosis and Cardiovascular DiseasesAutophagy in Disease and TherapyCell death mechanisms and regulation

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Vascular smooth muscle cell death, autophagy and senescence in atherosclerosis

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Grootaert, Mandy O J, Moulis, Manon, Roth, Lynn, Martinet, Wim, Vindis, Cécile, Bennett, Martin R, De Meyer, Guido R Y·2018·Cardiovascular Research

DOI 10.1093/cvr/cvy007

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Abstract

In the present review, we describe the causes and consequences of loss of vascular smooth muscle cells (VSMCs) or their function in advanced atherosclerotic plaques and discuss possible mechanisms such as cell death or senescence, and induction of autophagy to promote cell survival. We also highlight the potential use of pharmacological modulators of these processes to limit plaque progression and/or improve plaque stability. VSMCs play a pivotal role in atherogenesis. Loss of VSMCs via initiation of cell death leads to fibrous cap thinning and promotes necrotic core formation and calcification. VSMC apoptosis is induced by pro-inflammatory cytokines, oxidized low density lipoprotein, high levels of nitric oxide and mechanical injury. Apoptotic VSMCs are characterized by a thickened basal lamina surrounding the cytoplasmic remnants of the VSMC. Inefficient clearance of apoptotic VSMCs results in secondary necrosis and subsequent inflammation. A critical determinant in the VSMC stress response and phenotypic switching is autophagy, which is activated by various stimuli, including reactive oxygen and lipid species, cytokines, growth factors and metabolic stress. Successful autophagy stimulates VSMC survival, whereas reduced autophagy promotes age-related changes in the vasculature. Recently, an interesting link between autophagy and VSMC senescence has been uncovered. Defective VSMC autophagy accelerates not only the development of stress-induced premature senescence but also atherogenesis, albeit without worsening plaque stability. VSMC senescence in atherosclerosis is likely a result of replicative senescence and/or stress-induced premature senescence in response to DNA damaging and/or oxidative stress-inducing stimuli. The finding that VSMC senescence can promote atherosclerosis further illustrates that normal, adequate VSMC function is crucial in protecting the vessel wall against atherosclerosis.

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Additional file 2 of JIB-04, a histone demethylase Jumonji C domain inhibitor, regulates phenotypic switching of vascular smooth muscle cells
He, Y., Yi, X., Zhang, Z., Luo, H., Li, R., Feng, X., Fang, Z.-M., Zhu, X.-H., Cheng, W., Jiang, D.-S., et al. (2022) · Figshare · doi:10.6084/m9.figshare.20488409
Additional file 1 of SPAG5 deficiency activates autophagy to reduce atherosclerotic plaque formation in ApoE−/− mice
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Additional file 1 of Predictive effect of triglyceride-glucose index on clinical events in patients with acute ischemic stroke and type 2 diabetes mellitus
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Additional file 1 of Cigarette tar accelerates atherosclerosis progression via RIPK3-dependent necroptosis mediated by endoplasmic reticulum stress in vascular smooth muscle cells
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Authors: Grootaert, M. O. J., Moulis, M., Roth, L., Martinet, W., Vindis, C., Bennett, M. R., & De Meyer, G. R. Y.
Affiliations: University of Cambridge (GB)
Inserm (FR)
University of Antwerp (BE)
Laboratory of Physiopharmacology, University of Antwerp, Universiteitsplein 1, B-2610 Antwerp, Belgium
ORCID: Grootaert, Mandy O J
Moulis, Manon
Roth, Lynn
Martinet, Wim
Vindis, Cécile
Bennett, Martin R
Venue: Cardiovascular Research
Publisher: Oxford University Press (OUP)
Published: 2018-01-18
Volume: 114
Issue: 4
Pages: 622-634
ISSN: 0008-6363 (ISSN-L)
1755-3245
DOI: 10.1093/cvr/cvy007
OpenAlex: W2792785502
Cited by: 606
References: 95
Citations by year: 2026: 57 · 2025: 80 · 2024: 108 · 2023: 73 · 2022: 112 · 2021: 70 · 2020: 54 · 2019: 32 · 2018: 19
FWCI: 4.48
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Cardiovascular Research (publishedVersion)
PubMed (publishedVersion)
Lirias (KU Leuven) (submittedVersion, other-oa)
Digital Access to Libraries (submittedVersion, other-oa)
Funders: FWO (G.0412.16 N)
British Heart Foundation (RG/13/14/30314 and PG/16/11/32021)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: vascular smooth muscle cells, atherosclerosis, apoptosis, autophagy, cellular senescence, stress-induced premature senescence, replicative senescence, plaque stability, fibrous cap thinning, necrotic core, calcification, oxidized LDL, nitric oxide, inflammatory cytokines, autophagy modulators, VSMC phenotypic switching
MeSH terms: Animals, Arteries, Autophagy, Humans, Muscle, Smooth, Vascular, Phenotype, Signal Transduction, Cellular Senescence, Myocytes, Smooth Muscle, Cell Proliferation, Atherosclerosis, Plaque, Atherosclerotic

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Vascular smooth muscle cell death, autophagy and senescence in atherosclerosis

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