ArticleInvestigative ophthalmology & visual science2025
Palmitic Acid Induces Ferroptosis in Retinal Microvascular Endothelial Cells by Palmitoylation of Keap1 to Affect Diabetic Retinopathy.
Article in Investigative ophthalmology & visual science, 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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Who cites it
1 citing paper in PubMed.
- Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects.Frontiers in endocrinology · 2026Review
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Authors and funding
5 authors.
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Abstract
Purpose: Retinal microvascular endothelial cells (RMECs) injury caused by sustained hyperglycemia was the initial factor in diabetic retinopathy (DR). Here, we explored a novel mechanism by which palmitic acid (PA) contributed to RMEC damage in DR. Methods: Diabetic rats and high glucose (HG)-treated human RMECs (HRMECs) were used for the in vivo and in vitro experiments. The pathological changes of retinal tissues were evaluated by hematoxylin & eosin staining; mannose receptor (CD206) and B7-2 (CD86) expression were detected by immunohistochemical staining and flow cytometry; cell viability was measured using Cell Counting Kit-8; the protein levels were detected by Western blot. Results: Ferroptosis was induced in the retinal tissues of diabetic rats and HG-treated HRMECs, which was verified by increased kelch-like ECH-associated protein 1 (Keap1), acyl-CoA synthetase long-chain family member 4 (ACSL4), malondialdehyde (MDA), and reactive oxygen species (ROS) levels, whereas glutathione (GSH), nuclear factor erythroid 2-related factor 2 (Nrf2), and glutathione peroxidase 4 (GPX4) levels were decreased. PA exhibited the similar promotion effect on ferroptosis in HRMECs, which was reversed by 2-bromohexadecanoic acid and further enhanced by Palmostatin B. The palmitoylation modification of Keap1 in HRMECs was confirmed, and si-Keap1 reversed the increased Keap1, ACSL4, MDA and ROS, decreased Nrf2, GPX4 and GSH induced by PA. The in vivo experiments further revealed that si-Keap1 alleviated DR and reduced ferroptosis. Conclusions: These results suggested that PA induced Keap1 palmitoylation to upregulate Keap1 levels to inhibit Nrf2/GPX4 pathway, thus enhancing ferroptosis in HRMECs and aggravating DR.
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