ArticleInvestigative ophthalmology & visual science2026
Digoxin Attenuates Ocular Hypertension and Protects Trabecular Meshwork Cells via Ferroptosis Inhibition.
Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Unfolding Immune Dysregulation in COPD: Identification of a Three-Gene Signature and Functional Validation ofInternational journal of molecular sciences · 2026Article
- Ferroptosis and the eye: bridging the gap between cell death and vision preservation.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Emerging evidence implicates ferroptosis in trabecular meshwork (TM) injury during glaucoma pathogenesis. This study aims to systematically characterize ferroptosis-related gene signatures in primary open-angle glaucoma (POAG) and identify small-molecule therapeutics targeting this mechanism. Methods: We performed Mendelian randomization (MR) analysis of East Asian genome-wide association study data to assess causal relationships between blood metals and POAG. Ferroptosis-related indicators (iron ions, MDA, GPX4, GSH) were measured in aqueous humor samples from patients with POAG using ELISA. Genome-wide expression of TM from patients with POAG was integrated with ferroptosis-related gene sets (FerrDb) to identify core regulatory genes. The CMap database and molecular docking were employed to screen therapeutic compounds, with subsequent validation in hydrogen peroxide (H2O2)-induced TM ferroptosis models. Digoxin was formulated as topical ophthalmic drops and administered twice daily to chronic ocular hypertension (COH) rat models to evaluate its IOP-lowering efficacy. Results: MR analysis revealed that elevated serum iron levels causally increase POAG risk. Patients with POAG exhibited increased iron and MDA levels alongside decreased GPX4 and GSH. We identified 14 ferroptosis-related differentially expressed genes, with PPI analysis pinpointing SLC2A3, SCD, and HBA1 as hub genes linking ferroptosis to TM injury. Their dysregulation amplified lipid peroxidation cascades. CMap screening and molecular docking suggested ATPase inhibitor digoxin as a potential POAG therapeutic. Digoxin significantly attenuated H2O2-induced ferroptosis in HTMCs by reducing MDA and restoring GPX4, ultimately lowering IOP in COH eyes. Conclusions: Our findings establish digoxin as a promising therapeutic agent that suppresses ferroptosis and reduces IOP via the SLC2A3/SCD/HBA1 pathway, providing a transformative strategy for POAG treatment.
Indexed as
Identifiers
What Socratic holds
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.