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The cascade hypothesis of keratoconus.
M Cristina Kenney1, Donald J Brown
1Department of Ophthalmology, UCI Medical Center, University of California, Irvine, Building 55, Room 220, 101 The City Drive, Orange CA 92868, USA. mkenney@uci.edu
Summary
Keratoconus, a corneal thinning condition, may stem from defective enzymes causing oxidative damage. Patients should minimize UV exposure and eye rubbing to protect their corneas.
Area of Science:
- Ophthalmology
- Biochemistry
- Cell Biology
Background:
- Keratoconus is a progressive, non-inflammatory thinning of the cornea.
- It is a primary indication for corneal transplantation.
- The exact causes of keratoconus remain incompletely understood.
Purpose of the Study:
- To propose a novel "Cascade Hypothesis" for the causation of keratoconus.
- To explain the role of oxidative stress in keratoconus pathogenesis.
- To review supporting biochemical, immunohistochemical, and molecular data.
Main Methods:
- Review of existing biochemical data.
- Analysis of immunohistochemical findings.
- Evaluation of molecular biology studies.
Main Results:
- Keratoconus corneas exhibit abnormal enzymes in lipid peroxidation and/or nitric oxide pathways.
- This leads to oxidative damage and accumulation of cytotoxic by-products.
- Oxidative stress triggers a cascade of events including apoptosis, altered signaling, and fibrosis.
Conclusions:
- The "Cascade Hypothesis" provides a framework for understanding keratoconus development.
- Minimizing oxidative stress is crucial for keratoconus patients.
- Protective measures include UV protection, reduced eye rubbing, and proper eye care.