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Cited by 301

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Signaling mechanisms mediating vascular protective actions of vascular endothelial growth factor

Open access
Zachary, Ian·2001·American Journal of Physiology-Cell Physiology

Abstract

Vascular endothelial growth factor (VEGF) is essential for angiogenesis in health and pathophysiology, and it is currently a major focus for drug targeting in the development of treatments for diverse human diseases. Recently, we proposed that VEGF could also play a role as a vascular protective factor in the adult vasculature and in disease. In this model, vascular protection is defined as a VEGF-induced enhancement of endothelial functions that mediate the inhibition of vascular smooth muscle cell proliferation, enhanced endothelial cell survival, suppression of thrombosis, and anti-inflammatory effects. A feature of this model is that protective effects of VEGF are essentially independent of angiogenesis or endothelial cell proliferation. VEGF-dependent cell survival and VEGF-induced synthesis of nitric oxide and prostacyclin are likely to be key mediators of a vascular protective effect. Vascular protection should help to improve insight into the underlying mechanisms of cardiovascular actions of VEGF and prove valuable for developing novel therapeutic approaches to cardiovascular disease.

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Crossref · 10.1152/ajpcell.2001.280.6.c1375

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Metadata

Authors
Zachary, I.
Venue
American Journal of Physiology-Cell Physiology
Published
2001-06-01
Volume
280
Issue
6
Pages
C1375-C1386
ISSN
  • 0363-6143 (ISSN-L)
  • 1522-1563
OpenAlex
W2199292288
Cited by
301
References
5
FWCI
7.60
Type
journal article
Language
en
Open access
bronze

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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.