ArticleiScience2025
SH2B1 promotes apoptosis in diabetic cataract via p38 MAPK pathway.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- METTL16 Inhibits Lens Epithelial Cells Function in Diabetic Cataract via m6A-Modified DKK1-Mediated Wnt/β-Catenin Signaling.Investigative ophthalmology & visual science · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with diabetes face an increased risk of developing cataracts, with unclear mechanisms. Our study illuminates these mechanisms by identifying differentially expressed proteins in the lens anterior capsule of patients with diabetic cataract (DC) and age-related cataract using quantitative proteomics. We found SH2 domain-containing adapter protein B1 (SH2B1) to be crucial in DC progression. Reduced SH2B1 expression was confirmed through PCR and western blotting in patient samples, diet-induced obese mice, and high-glucose (HG)-cultured human lens epithelial cells. Under HG conditions, cell proliferation decreased, while migration and apoptosis, alongside changes in Bcl2 and caspase-3 expression, increased. Overexpressing SH2B1 alleviated these changes and influenced the p38 mitogen-activated protein kinase (MAPK) signaling pathway. This suggests SH2B1 and the p38 MAPK pathway as significant in DC pathogenesis and potential therapeutic targets. Clinically, this could lead to therapies aimed at halting or slowing DC progression.
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