The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
M-CSF inhibition selectively targets pathological angiogenesis and lymphangiogenesis
Open accessAbstract
Antiangiogenic therapy for the treatment of cancer and other neovascular diseases is desired to be selective for pathological angiogenesis and lymphangiogenesis. Macrophage colony-stimulating factor (M-CSF), a cytokine required for the differentiation of monocyte lineage cells, promotes the formation of high-density vessel networks in tumors and therefore possesses therapeutic potential as an M-CSF inhibitor. However, the physiological role of M-CSF in vascular and lymphatic development, as well as the precise mechanisms underlying the antiangiogenic effects of M-CSF inhibition, remains unclear. Moreover, therapeutic potential of M-CSF inhibition in other neovascular diseases has not yet been evaluated. We used osteopetrotic (op/op) mice to demonstrate that M-CSF deficiency reduces the abundance of LYVE-1+ and LYVE1− macrophages, resulting in defects in vascular and lymphatic development. In ischemic retinopathy, M-CSF was required for pathological neovascularization but was not required for the recovery of normal vasculature. In mouse osteosarcoma, M-CSF inhibition effectively suppressed tumor angiogenesis and lymphangiogenesis, and it disorganized extracellular matrices. In contrast to VEGF blockade, interruption of M-CSF inhibition did not promote rapid vascular regrowth. Continuous M-CSF inhibition did not affect healthy vascular and lymphatic systems outside tumors. These results suggest that M-CSF–targeted therapy is an ideal strategy for treating ocular neovascular diseases and cancer.
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Cites
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Cited by
Fantin, A., Vieira, J. M., Gestri, G., Denti, L., Schwarz, Q., Prykhozhij, S., Peri, F., Wilson, S. W., & Ruhrberg, C. (2010) · Blood · doi:10.1182/blood-2009-12-257832 · Cited by 1,153
The role of macrophage phenotype in vascularization of tissue engineering scaffolds
Spiller, K. L., Anfang, R. R., Spiller, K. J., Ng, J., Nakazawa, K. R., Daulton, J. W., & Vunjak-Novakovic, G. (2014) · Biomaterials · doi:10.1016/j.biomaterials.2014.02.012 · Cited by 948
The role of myeloid cells in cancer therapies
Engblom, C., Pfirschke, C., & Pittet, M. J. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.54 · Cited by 788
Macrophages in health and disease
Park, M. D., Silvin, A., Ginhoux, F., & Merad, M. (2022) · Cell · doi:10.1016/j.cell.2022.10.007 · Cited by 644
Ushach, I., & Zlotnik, A. (2016) · Journal of Leukocyte Biology · doi:10.1189/jlb.3ru0316-144r · Cited by 551
Metadata
- Authors
- Kubota, Y., Takubo, K., Shimizu, T., Ohno, H., Kishi, K., Shibuya, M., Saya, H., & Suda, T.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2009-04-27
- Volume
- 206
- Issue
- 5
- Pages
- 1089-1102
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2148596615
- Cited by
- 388
- References
- 7
- FWCI
- 10.92
- Type
- journal article
- Language
- en
- Open access
- green
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- Kubota, Y., Takubo, K., Shimizu, T., Ohno, H., Kishi, K., Shibuya, M., Saya, H., & Suda, T. (2009). M-CSF inhibition selectively targets pathological angiogenesis and lymphangiogenesis. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20081605
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