The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
VEGF-B is dispensable for blood vessel growth but critical for their survival, and VEGF-B targeting inhibits pathological angiogenesis
Open accessAbstract
VEGF-B, a homolog of VEGF discovered a long time ago, has not been considered an important target in antiangiogenic therapy. Instead, it has received little attention from the field. In this study, using different animal models and multiple types of vascular cells, we revealed that although VEGF-B is dispensable for blood vessel growth, it is critical for their survival. Importantly, the survival effect of VEGF-B is not only on vascular endothelial cells, but also on pericytes, smooth muscle cells, and vascular stem/progenitor cells. In vivo, VEGF-B targeting inhibited both choroidal and retinal neovascularization. Mechanistically, we found that the vascular survival effect of VEGF-B is achieved by regulating the expression of many vascular prosurvival genes via both NP-1 and VEGFR-1. Our work thus indicates that the function of VEGF-B in the vascular system is to act as a “survival,” rather than an “angiogenic” factor and that VEGF-B inhibition may offer new therapeutic opportunities to treat neovascular diseases.
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Cites
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Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene
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Angiogenesis as a therapeutic target
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Blocking Neuropilin-1 Function Has an Additive Effect with Anti-VEGF to Inhibit Tumor Growth
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Self-citationRissanen, T. T., Markkanen, J. E., Gruchala, M., Heikura, T., Puranen, A., Kettunen, M. I., Kholová, I., Kauppinen, R. A., Achen, M. G., Stacker, S. A., et al. (2003) · Circulation Research · doi:10.1161/01.res.0000073584.46059.e3 · Cited by 442
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Lee, C., Kim, M.-J., Kumar, A., Lee, H.-W., Yang, Y., & Kim, Y. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02249-0 · Cited by 365
Self-citationPostischemic Revascularization: From Cellular and Molecular Mechanisms to Clinical Applications
Silvestre, J.-S., Smadja, D. M., & Lévy, B. I. (2013) · Physiological Reviews · doi:10.1152/physrev.00006.2013 · Cited by 255
Genome-wide adaptive complexes to underground stresses in blind mole rats Spalax
Fang, X., Nevo, E., Han, L., Levanon, E. Y., Zhao, J., Avivi, A., Larkin, D., Jiang, X., Feranchuk, S., Zhu, Y., et al. (2014) · Nature Communications · doi:10.1038/ncomms4966 · Cited by 136
Pepe, M., Mamdani, M., Zentilin, L., Csiszar, A., Qanud, K., Zacchigna, S., Ungvari, Z., Puligadda, U., Moimas, S., Xu, X., et al. (2010) · Circulation Research · doi:10.1161/circresaha.110.220855 · Cited by 93
VEGF-B prevents excessive angiogenesis by inhibiting FGF2/FGFR1 pathway
Lee, C., Chen, R., Sun, G., Liu, X., Lin, X., He, C., Xing, L., Liu, L., Jensen, L. D., Kumar, A., et al. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01539-9 · Cited by 72
“Given that VEGF-B can be pro-2,5,40,41 or anti-angiogenic 8 – 10 (and current study) depending on the speci fi c context, outstanding questions thus exist.”
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Metadata
- Authors
- Zhang, F., Tang, Z., Hou, X., Lennartsson, J., Li, Y., Koch, A. W., Scotney, P., Lee, C., Arjunan, P., Dong, L., Kumar, A., Rissanen, T. T., Wang, B., Nagai, N., Fons, P., Fariss, R., Zhang, Y., Wawrousek, E., Tansey, G., Raber, J., Fong, G.-H., Ding, H., Greenberg, D. A., Becker, K. G., Herbert, J.-M., Nash, A., Yla-Herttuala, S., Cao, Y., Watts, R. J., & Li, X.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2009-04-14
- Volume
- 106
- Issue
- 15
- Pages
- 6152-6157
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1995150248
- Cited by
- 307
- References
- 28
- FWCI
- 8.28
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Zhang, F., Tang, Z., Hou, X., Lennartsson, J., Li, Y., Koch, A. W., Scotney, P., Lee, C., Arjunan, P., Dong, L., Kumar, A., Rissanen, T. T., Wang, B., Nagai, N., Fons, P., Fariss, R., Zhang, Y., Wawrousek, E., Tansey, G., . . . Li, X. (2009). VEGF-B is dispensable for blood vessel growth but critical for their survival, and VEGF-B targeting inhibits pathological angiogenesis. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0813061106
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
