Cited by 401Atherosclerosis and Cardiovascular DiseasesAngiogenesis and VEGF in CancerCerebrovascular and Carotid Artery Diseases

Angiogenesis in the atherosclerotic plaque

Open access
Camaré, Caroline, Pucelle, Mélanie, Nègre-Salvayre, Anne, Salvayre, Robert·2017·Redox Biology

Abstract

Atherosclerosis is a multifocal alteration of the vascular wall of medium and large arteries characterized by a local accumulation of cholesterol and non-resolving inflammation. Atherothrombotic complications are the leading cause of disability and mortality in western countries. Neovascularization in atherosclerotic lesions plays a major role in plaque growth and instability. The angiogenic process is mediated by classical angiogenic factors and by additional factors specific to atherosclerotic angiogenesis. In addition to its role in plaque progression, neovascularization may take part in plaque destabilization and thromboembolic events. Anti-angiogenic agents are effective to reduce atherosclerosis progression in various animal models. However, clinical trials with anti-angiogenic drugs, mainly anti-VEGF/VEGFR, used in anti-cancer therapy show cardiovascular adverse effects, and require additional investigations.

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Registry

Crossref · 10.1016/j.redox.2017.01.007

Cites

330 of 330 references verified0 citation errors · 0 not checkable

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  • Interaction between ECM on the surface of endothelial cells and integrins can initiate the intracellular PI3K-AKT-eNOS signaling pathway, leading to the production of NO.

    “It is well-documented that the interaction between the ECM on the surface of endothelial cells and integrins can initiate the intracellular PI3K-AKT-eNOS signaling pathway, leading to the production of NO.”

    From Decellularized liver scaffolds for constructing drug-metabolically functional ex vivo human liver models (2025) · cites this paper as [48]

    The NO/NOS discussion under “Classical factors involved in angiogenesis” (page not provided) says PI3K/Akt regulates endothelial eNOS and that eNOS generates NO. It does not say that ECM–integrin interactions initiate this pathway; the paper’s integrin discussion concerns targeted drug delivery instead. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • This enhancement is likely due to the activation of eNOS following the inoculation of endothelial cells onto the scaffold and their subsequent contact with the ECM, initiating a series of reactions that result in increased NO secretion.

    “This enhancement is likely due to the activation of eNOS following the inoculation of endothelial cells onto the scaffold and their subsequent contact with the ECM, initiating a series of reactions that result in increased NO secretion [47,48].”

    From Decellularized liver scaffolds for constructing drug-metabolically functional ex vivo human liver models (2025) · cites this paper as [48]

    The ‘Classical factors involved in angiogenesis’ section states that endothelial eNOS produces NO and that extracellular stimuli can regulate eNOS activity. It does not say that inoculating endothelial cells onto a scaffold or their contact with the ECM activates eNOS and increases NO secretion. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

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4 of the 334 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. [16]Geiringer E. Intimal vascularization and atherosclerosis J. Pathol. Bacteriol. 63 2 1951 201 211 14851161
  2. [50]van Uden P. Kenneth N.S. Rocha S. Regulation of hypoxia-inducible factor-1alpha by NF-kappaB Biochem. J. 412 3 2008 477 484 18393939 PMC2474706

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Authors
Camaré, C., Pucelle, M., Nègre-Salvayre, A., & Salvayre, R.
Affiliations
  • Université Toulouse III - Paul Sabatier (FR)
  • Inserm (FR)
Venue
Redox Biology
Publisher
Elsevier BV
Published
2017-08
Volume
12
Pages
18-34
ISSN
2213-2317 (ISSN-L)
OpenAlex
W2585441851
Cited by
401
References
334
Citations by year
2026: 18 · 2025: 39 · 2024: 61 · 2023: 62 · 2022: 49 · 2021: 55 · 2020: 44 · 2019: 36 · 2018: 28 · 2017: 9
FWCI
3.29
Type
journal article
Language
en
Open access
Locations
  • Redox Biology (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Institut National de la Santé et de la Recherche Médicale
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cerebrovascular and Carotid Artery Diseases
Keywords
angiogenesis, atherosclerosis, atherosclerotic plaque, neovascularization, plaque vulnerability, anti-angiogenic therapy, vascular endothelial growth factor, VEGFR, atherothrombosis, thromboembolism, inflammation, cholesterol accumulation
MeSH terms
Animals, Clinical Trials as Topic, Humans, Neovascularization, Pathologic, Oxidative Stress, Disease Progression, Angiogenesis Inhibitors, Plaque, Atherosclerotic

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