Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2010, Article ID 546826, 14 pages
Review Article

Inflammatory Mediators and Angiogenic Factors in Choroidal Neovascularization: Pathogenetic Interactions and Therapeutic Implications

1Department of Ophthalmology, University of Ferrara, Corso Giovecca 203, 44121 Ferrara, Italy
2St Paul's Eye Unit, Royal Liverpool University Hospital, Liverpool, UK
3Department of Health Sciences, University of Molise, Campobasso, Italy
4Department of Ophthalmology, University of Brescia, Brescia, Italy
5Center for Retinitis Pigmentosa of Veneto Region, ULSS 15 Alta Padovana, Camposampiero Hospital, Camposampiero, Italy

Received 11 March 2010; Accepted 2 July 2010

Academic Editor: F. D'Acquisto

Copyright © 2010 Claudio Campa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Choroidal neovascularization (CNV) is a common and severe complication in heterogeneous diseases affecting the posterior segment of the eye, the most frequent being represented by age-related macular degeneration. Although the term may suggest just a vascular pathological condition, CNV is more properly definable as an aberrant tissue invasion of endothelial and inflammatory cells, in which both angiogenesis and inflammation are involved. Experimental and clinical evidences show that vascular endothelial growth factor is a key signal in promoting angiogenesis. However, many other molecules, distinctive of the inflammatory response, act as neovascular activators in CNV. These include fibroblast growth factor, transforming growth factor, tumor necrosis factor, interleukins, and complement. This paper reviews the role of inflammatory mediators and angiogenic factors in the development of CNV, proposing pathogenetic assumptions of mutual interaction. As an extension of this concept, new therapeutic approaches geared to have an effect on both the vascular and the extravascular components of CNV are discussed.