Hypoxia in the pathogenesis of retinal disease

Abstract

Oxygen cannot passively diffuse for more than a radius of 100 μm around capillaries. As a result, adequate O2 supply to each cell depends on effective regulation of the integrity and function of the vascular network. On the other hand, high O2 tissue levels would result in reactive oxygen species (ROS) generation and cellular damage. Therefore, an optimal O 2 concentration is needed to avoid hypoxia or ROS-mediated cellular injury. The retinal tissue is very active metabolically and, therefore, exquisitely dependent on adequate O2 supply for its function [4]. The delivery of oxygen to the retina is dependent not only on systemic blood pressure, hemoglobin content and integrity of local vasculature, but on the level of intraocular pressure and local autoregulatory mechanisms as well. Hypoxia and its sequelae are implicated in the pathogenesis of most retinal diseases, especially those that involve pathologic neovascularization. This is due to the potent stimulation of production of vascular endothelial growth factor (VEGF), mediated by the hypoxia-inducible factor (HIF)-1 pathway, in response to hypoxia. © 2007 Springer-Verlag Berlin Heidelberg.