ArticleIranian journal of basic medical sciences2026
Melatonin alleviates ferroptosis in lens epithelial cells via regulating METTL14 expression.
Article in Iranian journal of basic medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: Ferroptosis in lens epithelial cells (LECs) is increasingly recognized as a key pathological process in cataract formation, driven by oxidative stress, lipid peroxidation, and aberrant RNA modification. This study investigated the role of METTL14 in UVB-induced ferroptosis in LECs and explored the protective mechanism of melatonin (MT). Materials and Methods: mRNA and protein levels of METTL14 and ferroptosis-related markers (GPX4, SLC7A11) were quantified. Lipid reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione levels were measured to assess ferroptotic activity. Mitochondrial structure and function were evaluated using transmission electron microscopy, mitochondrial membrane potential analysis, and ATP quantification. Results: UVB irradiation significantly up-regulated METTL14 expression and promoted ferroptosis in LECs. MT treatment reduced METTL14 expression, suppressed ferroptosis Conclusion: MT inhibits METTL14-mediated ferroptosis in LECs, reduces lipid peroxidation, and restores mitochondrial function, thereby slowing cataract progression. These findings highlight METTL14 as a critical regulator of ferroptosis and support MT as a promising therapeutic strategy for cataract prevention and treatment.
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