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Hypoxia-Inducible Factor 1 in the Glaucomatous Retina and Optic Nerve Head

Gülgün Tezel, MD; Martin B. Wax, MD

Arch Ophthalmol. 2004;122:1348-1356.

Objective  To examine tissue hypoxia in the retina and optic nerve head of glaucomatous eyes by the assessment of a transcription factor, hypoxia-inducible factor 1 (HIF-1), which is tightly regulated by the cellular oxygen concentration.

Methods  Using immunohistochemical analysis, the cellular localization of HIF-1 was studied in the retina and optic nerve head of 28 human donor eyes with glaucoma compared with 20 control eyes from healthy donors matched for several characteristics. The relationship between the retinal regions that exhibited immunostaining for HIF-1 and functional damage was examined using visual field data.

Results  There was an increase in the immunostaining for HIF-1 in the retina and optic nerve head of glaucomatous donor eyes compared with the control eyes. In addition, the retinal location of the increased immunostaining for HIF-1 in some of the glaucomatous eyes was closely concordant with the location of visual field defects recorded in these eyes.

Conclusions  Because the regions of HIF-1 induction represent the areas of decreased oxygen delivery and hypoxic stress, information obtained from this study provides direct evidence that tissue hypoxia is present in the retina and optic nerve head of glaucomatous eyes, and hypoxic signaling is a likely component of the pathogenic mechanisms of glaucomatous neurodegeneration.

Clinical Relevance  These findings support the presence of tissue hypoxia in the retina and optic nerve head of glaucomatous patients.

From the Department of Ophthalmology and Visual Sciences and Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, Ky (Dr Tezel); Alcon Laboratories, Ft Worth, Tex (Dr Wax); and Department of Ophthalmology, University of Texas Southwestern Medical School, Dallas (Dr Wax). The authors have no relevant financial interest in this article.

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