Cellular and Molecular Biology


Intraocular neovascularization

A. Yoshida, S. Yoshida, T. Ishibashi and H. Inomata

Department of Ophthalmology, Faculty of Medicine, Kyushu University, Fukuoka, Japan

Offprint requests to: Ayako Yoshida, MD, Department of Ophthalmology, University of Michigan, Kellogg Eye Center, 1000 Wall Street, Ann Arbor, MI 48105, USA


Summary. An important character of the eye is transparency, so intraocular neovascularization, which is fragile and likely to result in hemorrhage, would cause a functional disorder of the eye and contribute to loss of vision associated with such diseases as retinopathy of prematurity, diabetic retinopathy, retinal vein occlusion, and age-related macular degeneration. Recently interest in the mechanisms of intraocular neovascularization has increased, and the mechanisms have been gradually elucidated using several in vitro and in vivo angio-genesis models. Blood vessels in the eye are composed of, and surrounded by, various types of cells that produce multiple factors. Neovascularization is regulated by complex interactions among these angiogenic factors, angiostatic factors, and adhesion molecules, and some of these angiogenesis-related molecules have also been suggested as new targets for novel therapeutic agents of intraocular neo-vascularization. This review focuses on in vivo representative angiogenesis models of the corneal pocket model and the model of oxygen-induced retinopathy, and discusses the role of some angiogenesis-related factors and adhesion molecules in intraocular neovascularization. Histol. Histopathol. 14, 1287-1294 (1999)

Key words: Neovascularization, vascular endothelial growth factor/vascular permeability factor, Interleukin-8, NF-kB, Adhesion molecule

DOI: 10.14670/HH-14.1287