Emerging roles of oxidative stress in the pathogenesis of pseudoexfoliation syndrome (Review)
- Stylianos Mastronikolis
- Marina Pagkalou
- Panagiotis Plotas
- Konstantinos Kagkelaris
- Constantinos D. Georgakopoulos
Affiliations: Department of Ophthalmology, University Hospital of Patras, 26504 Patras, Greece, Department of Chemistry, University of Crete, 70013 Heraklion, Greece, Laboratory of Primary Health Care, School of Health Rehabilitation Sciences, University of Patras, 26334 Patras, Greece
- Published online on: July 28, 2022 https://doi.org/10.3892/etm.2022.11539
Copyright: © Mastronikolis
et al. This is an open access article distributed under the
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Commons Attribution License.
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Pseudoexfoliation syndrome (PEXS) is a systemic disease caused by defects in the extracellular matrix (ECM) remodelling process leading to the chronic deposition of extracellular, fibrillary, white flaky pseudoexfoliation material (PEXM) throughout the body. Specifically, PEXM deposits on the lens capsule cause open‑angle glaucoma, cataracts and blindness in patients with PEXS. Several gene single nucleotide polymorphisms are linked to the development of PEXS in humans, including lysyl oxidase‑like 1 gene, clusterin and fibulin‑5. The exact reason for the PEXM generation and its resulting pathogenesis is not well understood. However, defective ECM remodelling and oxidative stress (OS) have been hypothesized as significant events leading to the PEXM. Specifically, the link between OS and PEXS has been well studied, although the investigation is still ongoing. The present review explored recent advances in various aspects of PEXS and the involvement of OS in the eye for PEXS development.