Angiogenesis: Insights from a Systematic Overview by Gaetano Santulli

By Gaetano Santulli

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Most previous efforts have thus been focused on developing anti-angiogenic agents that primarily target ECs. The recent clinical experience with VEGF inhibitors has provided a number of important, but puzzling, insights and raised various outstanding questions. First, the anti-VEGF antibody Avastin 24 Evangeli Lampri and Elli Ioachim (Genentech) only provides an overall survival benefit in colorectal, breast and lung cancer patients when combined with conventional chemotherapy. Unfortunately, clinical trials testing mainly the pro-angiogenic potential of VEGF have not had the expected results.

UPA), whilst, at high doses, TGF-b1 contributes to the resolution of angiogenesis, by inhibiting EC proliferation and migration, by promoting the reformation of the basement membrane, and by stimulating the recruitment of mesenchymal cells (via upregulation of PDGF-B) and their differentiation to SMC (via upregulation of SM22a). Interpretations differ, however, about the respective signalling roles of ALK-1 (and downstream Smad 1/5) and ALK-5 (and Smad 2/3) in the activation or resolution phase of angiogenesis.

Consequently the net expression of these two receptors and their respective target Smads dictates the end result of TGF-beta response in endothelial cells. [3, 12, 102] There is also endoglin, a type III receptor, which facilitates binding of TGF-b1 to the type II receptors. Both pro- and anti-angiogenic properties have been ascribed to TGF-b1 – resulting from effects on EC and other cell types. g. g. uPA), whilst, at high doses, TGF-b1 contributes to the resolution of angiogenesis, by inhibiting EC proliferation and migration, by promoting the reformation of the basement membrane, and by stimulating the recruitment of mesenchymal cells (via upregulation of PDGF-B) and their differentiation to SMC (via upregulation of SM22a).

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