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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
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