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Pathophysiological consequences of VEGF-induced vascular permeability

Author

Listed:
  • Sara M. Weis

    (University of California, San Diego)

  • David A. Cheresh

    (University of California, San Diego)

Abstract

Although vascular endothelial growth factor (VEGF) induces angiogenesis, it also disrupts vascular barrier function in diseased tissues. Accordingly, VEGF expression in cancer and ischaemic disease has unexpected pathophysiological consequences. By uncoupling endothelial cell–cell junctions VEGF causes vascular permeability and oedema, resulting in extensive injury to ischaemic tissues after stroke or myocardial infarction. In cancer, VEGF-mediated disruption of the vascular barrier may potentiate tumour cell extravasation, leading to widespread metastatic disease. Therefore, by blocking the vascular permeability promoting effects of VEGF it may be feasible to reduce tissue injury after ischaemic disease and minimize the invasive properties of circulating tumour cells.

Suggested Citation

  • Sara M. Weis & David A. Cheresh, 2005. "Pathophysiological consequences of VEGF-induced vascular permeability," Nature, Nature, vol. 437(7058), pages 497-504, September.
  • Handle: RePEc:nat:nature:v:437:y:2005:i:7058:d:10.1038_nature03987
    DOI: 10.1038/nature03987
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    Cited by:

    1. Judy R. Beijnum & Elisabeth J. M. Huijbers & Karlijn Loon & Athanasios Blanas & Parvin Akbari & Arno Roos & Tse J. Wong & Stepan S. Denisov & Tilman M. Hackeng & Connie R. Jimenez & Patrycja Nowak-Sli, 2022. "Extracellular vimentin mimics VEGF and is a target for anti-angiogenic immunotherapy," Nature Communications, Nature, vol. 13(1), pages 1-20, December.
    2. Kang Qi & Lujin Li & Xiangdong Li & Jinglin Zhao & Yang Wang & Shijie You & Fenghuan Hu & Haitao Zhang & Yutong Cheng & Sheng Kang & Hehe Cui & Lian Duan & Chen Jin & Qingshan Zheng & Yuejin Yang, 2015. "Cardiac Microvascular Barrier Function Mediates the Protection of Tongxinluo against Myocardial Ischemia/Reperfusion Injury," PLOS ONE, Public Library of Science, vol. 10(3), pages 1-24, March.

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