ArticleInvestigative ophthalmology & visual science2025
Simvastatin-Induced Ferroptosis in Orbital Fibroblasts in Graves' Ophthalmopathy.
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 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.
- MicroRNAs in thyroid eye disease: expression signatures and clinical implications.Frontiers in immunology · 2026Review
- Unravelling the pathogenic mechanisms in Graves' orbitopathy.European thyroid journal · 2025Review
- Research progress on ferroptosis and PARP inhibitors in ovarian cancer: action mechanisms and resistance mechanisms.Frontiers in pharmacology · 2025Review
- Ferroptosis in ocular diseases: mechanisms, crosstalk with other cell death pathways, and therapeutic prospects.Frontiers in medicine · 2025Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Graves' ophthalmopathy (GO), the most common extrathyroidal manifestation of Graves' disease, is disabling and disfiguring. Recent studies have shown that statins have a protective effect on individuals with GO. Statins were reported to trigger ferroptosis in some disorders, but little is known about whether statins protect against GO via ferroptosis. The aim of this study was to explore whether ferroptosis is involved in the protective effect of simvastatin on GO. Methods: GO-OFs, which are orbital fibroblasts (OFs) derived from individuals with GO, were analyzed for lipogenesis by RT-qPCR and Red Oil O staining posttreatment with simvastatin. CCK-8 assays, flow cytometric analysis, and transmission electron microscopy (TEM) were used to compare the sensitivity of GO-OFs and control-OFs to erastin-induced ferroptosis. The ferroptosis levels in the GO-OFs were evaluated by measuring cell viability, reactive oxygen species (ROS) levels, and lipid peroxidation levels and performing TEM analysis after treatment with simvastatin and Fer-1. Results: The GO-OFs were resistant to erastin-induced ferroptosis. The viability and lipogenesis of the GO-OFs were significantly decreased, while the levels of ROS, lipid peroxidation, and the ferroptosis marker ACLS4 were increased upon treatment with simvastatin. Conclusions: Our study indicated that ferroptosis plays an important role in the pathogenesis of GO and that simvastatin may induce ferroptosis, suggesting that this drug could serve as a novel therapeutic agent for GO.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.