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Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis
Open accessAbstract
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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“Small-molecule drugs like the fumagillin analogue TNP-470, endostatin or angiostatin reduced plaque angiogenesis and inhibited advanced atherosclerosis in APOE-knockout mice after prolonged treatment for 16 weeks105,106.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [106]
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Metadata
- 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)
- 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
- 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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