Chemokines as mediators of neovascularization
Open accessAbstract
Chemokines are a superfamily of homologous heparin-binding proteins, first described for their role in recruiting leukocytes to sites of inflammation. Chemokines have since been recognized as key factors mediating both physiological and pathological neovascularization in such diverse clinical settings as malignancy, wound repair, chronic fibroproliferative disorders, myocardial ischemia, and atherosclerosis. Members of the CXC chemokine family, structurally defined as containing the ELR amino acid motif, are potent inducers of angiogenesis, whereas another subset of the CXC chemokines inhibits angiogenesis. In addition, CCL2, a CC chemokine ligand, has been implicated in arteriogenesis. In this article, we review the current literature on the role of chemokines as mediators of neovascularization.
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CXCL9 inhibits neovascularization.
“CXCL9 also inhibits neovascularization (83) and has anti-tumor and anti-metastatic effects (74).”
From Macrophage Cytokines: Involvement in Immunity and Infectious Diseases (2014) · cites this paper as [83]
CXCL10 is secreted by monocytes, macrophages, fibroblasts, and endothelial cells.
“CXCL10, or interferon gamma-induced protein 10, is secreted not only by monocytes and macrophages, but also by fibroblasts and endothelial cells (83).”
From Macrophage Cytokines: Involvement in Immunity and Infectious Diseases (2014) · cites this paper as [83]
The Introduction identifies CXCL10 as IP-10 and says it is induced by interferons, but it does not identify which cells secrete it. Searches for CXCL10 production or secretion by monocytes, macrophages, fibroblasts, and endothelial cells found no passage in our copy addressing that claim. (LLM, conf=0.72)
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- Authors
- Keeley, E. C., Mehrad, B., & Strieter, R. M.
- Affiliations
- University of Virginia (US)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2008-11
- Volume
- 28
- Issue
- 11
- Pages
- 1928-1936
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC2735456
- OpenAlex
- W2125050685
- Cited by
- 192
- References
- 142
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 7 · 2022: 10 · 2021: 17 · 2020: 7 · 2019: 6 · 2018: 12 · 2017: 7 · 2016: 6 · 2015: 14 · 2014: 12 · 2013: 15 · 2012: 19
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL66027, HL-73848, R01HL066027, R01HL073848)
- National Cancer Institute (CA-87879, R01CA087879)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Keywords
- chemokines, neovascularization, angiogenesis, arteriogenesis, CXC chemokines, CC chemokines, MCP-1, inflammation, wound healing, atherosclerosis, myocardial ischemia, fibroproliferative disorders, cancer
- MeSH terms
- Animals, Humans, Neovascularization, Pathologic, Neovascularization, Physiologic, Chemokines, Angiogenic Proteins, Endothelial Cells, Angiostatic Proteins
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