gms | German Medical Science

24th Annual Meeting of the German Retina Society

German Retina Society

17.06. - 18.06.2011, Aachen

Systemic anti-VEGF actions

Meeting Abstract

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  • Johannes Waltenberger - Klinik und Poliklinik für Kardiologie, Universitätsklinikum Münster

German Retina Society. 24th Annual Conference of the German Retina Society. Aachen, 17.-18.06.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11rg08

doi: 10.3205/11rg08, urn:nbn:de:0183-11rg088

This is the translated version of the article.
The original version can be found at: http://www.egms.de/de/meetings/rg2011/11rg08.shtml

Published: June 15, 2011

© 2011 Waltenberger.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

VEGF is a central endothelial and angiogenic peptide growth factor. In the past 2 decades, various functions of VEGF (generally referred to as VEGF-A165) and its relatives (VEGF-B, VEGF-C, VEGF-D, VEGF-E, PlGF-1, PlGF-2) and their central importance for different aspects of endothelial function have been described and characterized. All possible side effect of therapeutic VEGF inhibition can be explained by the inhibition of VEGF action.VEGF actions on the endothelium are: stimulation of migration, stimulation of proliferation, anti-hrombotic action, anti-apoptotic action, anti-proliferative for smooth muscle cells secondary to the release of nitric oxide (NO) and prostacyclin (PGI2), regulation of permeability, release of endothelial cells from the bone marrow and stimulation of their ability to home at sites of endothelial repair. Based on these actions of VEGF, possible side effects of anti-VEGF treatment are: endothelial dysfunction, arterial hypertension and blood pressure crises, vascular regression, capillary bleeding, atherosclerotic plaque rupture triggering ischemic complications such as myocardial infarction or stroke. Taken together, the therapeutic inhibition of VEGF action can lead to multiple and relevant important systemic side effects based on fundamental involvement of VEGF in endothelial physiology.