Cited by 652Atherosclerosis and Cardiovascular DiseasesCholesterol and Lipid MetabolismCerebrovascular and Carotid Artery Diseases

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Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis

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Moulton, Karen S., Vakili, Khashayar, Zurakowski, David, Soliman, Mohsin, Butterfield, Catherine, Sylvin, Erik, Lo, Kin-Ming, Gillies, Stephen, Javaherian, Kashi, Folkman, Judah·2003·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0730843100PMC PMC153625

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Abstract

Plaque angiogenesis promotes the growth of atheromas, but the functions of plaque capillaries are not fully determined. Neovascularization may act as a conduit for the entry of leukocytes into sites of chronic inflammation. We observe vasa vasorum density correlates highly with the extent of inflammatory cells, not the size of atheromas in apolipoprotein E-deficient mice. We show atherosclerotic aortas contain activities that promote angiogenesis. The angiogenesis inhibitor angiostatin reduces plaque angiogenesis and inhibits atherosclerosis. Macrophages in the plaque and around vasa vasorum are reduced, but we detect no direct effect of angiostatin on monocytes. After angiogenesis blockade in vivo , the angiogenic potential of atherosclerotic tissue is suppressed. Activated macrophages stimulate angiogenesis that can further recruit inflammatory cells and more angiogenesis. Our findings demonstrate that late-stage inhibition of angiogenesis can interrupt this positive feedback cycle. Inhibition of plaque angiogenesis and the secondary reduction of macrophages may have beneficial effects on plaque stability.

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Authors: Moulton, K. S., Vakili, K., Zurakowski, D., Soliman, M., Butterfield, C., Sylvin, E., Lo, K.-M., Gillies, S., Javaherian, K., & Folkman, J.
Affiliations: Boston University (US)
ORCID: Moulton, Karen S.
Vakili, Khashayar
Zurakowski, David
Lo, Kin-Ming
Gillies, Stephen
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2003-04-07
Volume: 100
Issue: 8
Pages: 4736-4741
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.0730843100
PMC: PMC153625
OpenAlex: W2146672236
Semantic Scholar: 82c000d66a80c8c81b76c493b4ef41413cde3f9b
Cited by: 652
References: 32
Citations by year: 2026: 3 · 2025: 9 · 2024: 12 · 2023: 15 · 2022: 15 · 2021: 16 · 2020: 18 · 2019: 19 · 2018: 13 · 2017: 19 · 2016: 35 · 2015: 29 · 2014: 35 · 2013: 30 · 2012: 27
FWCI: 14.61
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute
Topics: Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cerebrovascular and Carotid Artery Diseases
Keywords: atherosclerosis, plaque neovascularization, angiogenesis inhibition, angiostatin, macrophage accumulation, vasa vasorum, ApoE-deficient mice, plaque stability, chronic inflammation, leukocyte recruitment, positive feedback loop
MeSH terms: Animals, Apolipoproteins E, Arteriosclerosis, Feedback, Inflammation, Lymphokines, Macrophages, Mice, Inbred C57BL, Monocytes, Neovascularization, Pathologic, Peptide Fragments, Plasminogen, Receptors, LDL, Vasa Vasorum, Endothelial Growth Factors, Mice, Knockout, Chemokine CCL2, Intercellular Signaling Peptides and Proteins, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Angiostatins, Mice, In Vitro Techniques

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Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis

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