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REVIEW ARTICLE
Year : 2015  |  Volume : 10  |  Issue : 1  |  Page : 60-67

Cytochrome P450 1B1 and primary congenital glaucoma


1 Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
2 Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI; McPherson Eye Research Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
3 Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI; McPherson Eye Research Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA

Correspondence Address:
Nader Sheibani
Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, 1111 Highland Avenue, 9453 WIMR, Madison, WI 53705
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2008-322X.156116

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Cytochrome P450 1B1 (Cyp1b1) belongs to the CYP450 superfamily of heme-binding mono-oxygenases which catalyze oxidation of various endogenous and exogenous substrates. The expression of Cyp1b1 plays an important role in the modulation of development and functions of the trabecular meshwork (TM). Mutations in Cyp1b1 have been reported in patients with primary congenital glaucoma (PCG). Mice lacking Cyp1b1 also exhibit developmental defects in the TM similar to those reported in congenital glaucoma patients. However, how Cyp1b1 deficiency contributes to TM dysgenesis remains unknown. In the present review, we will address the significance of Cyp1b1 expression and/or its function in anterior segment development. Cyp1b1-deficient ( Cyp1b1−/−) mice are discussed as a promising model for an oxidative stress-induced model of PCG, in which Cyp1b1 activity is revealed as an important modulator of oxidative homeostasis contributing to the development and structural function of the TM. This conclusion suggests a possible clinical intervention for individuals who are genetically at high risk of developing PCG.


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