ArticleExperimental and therapeutic medicine2017
Immunohistochemical analysis of microsomal glutathione S-transferase 1 and clusterin expression in lens epithelial cells of patients with pseudoexfoliation syndrome.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- METTL5 promotes tumor progression and ferroptosis resistance via MGST1 in HCC.Molecular and cellular biochemistry · 2026Article
- Antioxidant Defense and Pseudoexfoliation Syndrome: An Updated Review.Medical sciences (Basel, Switzerland) · 2022Review
- Emerging roles of oxidative stress in the pathogenesis of pseudoexfoliation syndrome (Review).Experimental and therapeutic medicine · 2022Review
- Pseudoexfoliation and Cataract Syndrome Associated with Genetic and Epidemiological Factors in a Mayan Cohort of Guatemala.International journal of environmental research and public health · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudoexfoliation syndrome (PEX) is an age-associated, sight disorder affecting elastic fibers in the eye and visceral organs but its exact etiology remains unknown. The purpose of the current study was to determine the morphology and ultrastructure of lens epithelial cells (LECs), and to use immunohistochemistry to examine localization of microsomal glutathione S-transferase 1 (MGST1) and clusterin. Anterior lens capsules were obtained from 24 patients (13 PEX and 11 controls) who underwent phacoemulsification. Immunohistochemistry was performed, using antibodies against MGST1 and clusterin, to determine their expression. The morphology and ultrastructure of LECs were evaluated by light and transmission electron microscopy, respectively. The PEX LECs were characterized by significantly lower MGST1 (P=0.0001) and clusterin expression (P=0.0005) compared with the control group patients. PEX LECs were also observed to have significantly increased thickness compared with the control group patients (P=0.0002). The current findings suggest that low MGST1 and clusterin expression levels may be an early clinical indicator of PEX, and that oxidative stress may serve an important role, but that the specific etiology of this disease has yet to be revealed.
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