VEGF/VEGFR signalling as a target for inhibiting angiogenesis

Abstract

VEGFs and a respective family of tyrosine kinases receptors (VEGFRs) are key proteins modulating angiogenesis, the formation of new vasculature from an existing vascular network. There has been considerable evidence in vivo, including clinical observations, that abnormal angiogenesis is implicated in a number of disease conditions, which include rheumatoid arthritis, inflammation, cancer, psoriasis, degenerative eye conditions and others. Antiangiogenic therapies based on inhibition of VEGF/VEGFR signalling were reported to be powerful clinical strategies in oncology and ophthalmology. Current efforts have yielded promising clinical data for several antiangiogenic therapeutics. In this review, the authors elucidate key aspects of VEGFR signalling, as well as clinically relevant strategies for the inhibition of VEGF-induced angiogenesis, with an emphasis on small-molecule VEGFR inhibitors.

Synergistic Binding of Vascular Endothelial Growth Factor-A and Its Receptors to Heparin Selectively Modulates Complex Affinity

“…after myocardial infarction, stroke, diabetic ulcers, etc.) and to inhibit tumor growth and vision loss (8). However, the lack of a detailed understanding of all the factors that control the balance of the angiogenic signal has significantly limited the potential for designing efficient therapies for directing angiogenesis.…”

Emodin Inhibits Proinflammatory Responses and Inactivates Histone Deacetylase 1 in Hypoxic Rheumatoid Synoviocytes

“…[4][5][6] VEGF level is significantly high in RA synovial fluid. 7) Blocking VEGF using VEGF inhibitors 8,9) or small interfering RNA (siRNA) for VEGF receptor 2 (VEGFR2) suppressed secretion of proinflammatory cytokines that indirectly contribute to inhibit angiogenesis. 10) In addition, angiogenesis promoted by VEGF stimulates the release of proinflammatory mediators such as cyclooxygenase 2 (COX-2), 8) matrix metalloproteinases (MMPs) 11) and inducible nitric oxide synthase (iNOS).…”

Effect of Shenqin biochemical extract on hypoxia-inducible factor-1α expression in ultraviolet B-irradiated HaCaT cells

“…UVB radiation can cause skin damage, aging, and even cancer. It can lead to point mutations in the tumor-suppressor gene p53, and p53 and HIF-1α can affect each other (Kiselyov et al, 2007;Heidenreich et al, 2009).…”