ArticleIndian journal of ophthalmology2026
Notch 3 regulates ferroptosis of lens epithelial cells in age-related cataract by PI3K/AKT pathway.
Article in Indian journal of ophthalmology, 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
purposeAge-related cataract (ARC) is one of the leading causes of blindness and visual impairment globally. The aim of this study was to explore the role of Notch 3 in ARC as well as the mechanisms underlying Notch 3 in ARC.
methodsAn in vitro model was established to mimick the microenvironment of ARC, the lens epithelial cell line (LEC) B3 were treated with hydrogen peroxide (H2O2) once they reached approximately 80% confluence. Cell Counting Kit-8 (CCK-8) assay was performed to evaluate the proliferation of LEC B3. The mRNA of Notch 3 was detected via RNA extraction and quantitative real-time PCR (RT-qPCR). The protein level of Notch 3 was measured by western blot.
resultsThe mRNA and protein expression of Notch 3 were evidently down-regulated in H2O2-inducted LEC B3. Overexpression of Notch 3 increased the proliferation and suppressed the apoptosis of H2O2-inducted LECs B3. The elevated level of Notch 3 decreased the reactive oxygen species (ROS) fluorescence intensity and decreased Fe2+ and total Fe levels. In addition, Notch 3 up-regulation increased the levels of ferroptosis-related proteins GPX4 and SLC7A11. Notch 3 overexpression decreased the protein levels of p-PI3K, and p-AKT in H2O2-treated LECs B3. PI3K/AKT pathway inhibitor reversed the role effect of Notch 3 overexpression on the proliferation, apoptosis, and ferroptosis of LECs cells in ARC model.
conclusionThe present study identified that Notch 3 regulates ferroptosis of LECs B3 in ARC by PI3K/AKT pathway, which might offer a novel biomarker for the future investigation of the target of ARC.
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