期刊
JOURNAL OF INTERNAL MEDICINE
卷 273, 期 2, 页码 114-127出版社
WILEY
DOI: 10.1111/joim.12019
关键词
angiogenesis; signal transduction; tumours; vascular permeability; VEGFA; VEGFR2
资金
- Swedish Research Council
- Swedish Cancer Foundation
- Knut and Alice Wallenberg Foundation
Claesson-Welsh L, Welsh M (Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden and Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden). VEGFA and tumour angiogenesis (Review). J Intern Med 2013; 273: 114-127. In this review we summarize the current understanding of signal transduction downstream of vascular endothelial growth factor A (VEGFA) and its receptor VEGFR2, and the relationship between these signal transduction pathways and the hallmark responses of VEGFA, angiogenesis and vascular permeability. These physiological responses involve a number of effectors, including extracellular signal-regulated kinases (ERKs), Src, phosphoinositide 3 kinase (PI3K)/Akt, focal adhesion kinase (FAK), Rho family GTPases, endothelial NO and p38 mitogen-activated protein kinase (MAPK). Several of these factors are involved in the regulation of both angiogenesis and vascular permeability. Tumour angiogenesis primarily relies on VEGFA-driven responses, which to a large extent result in a dysfunctional vasculature. The reason for this remains unclear, although it appears that certain aspects of the VEGFA-stimulated angiogenic milieu (high level of microvascular density and permeability) promote tumour expansion. The high degree of redundancy and complexity of VEGFA-driven tumour angiogenesis may explain why tumours commonly develop resistance to anti-angiogenic therapy targeting VEGFA signal transduction.
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