ArticleCell death discovery2025
Metformin protects retinal ganglion cells in a preclinical model of retinal ischemia/reperfusion injury and stabilizes visual field in diabetic patients with glaucoma.
Article in Cell death discovery, 2025. 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
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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.
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.
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Who cites it
2 citing papers in PubMed.
- Peripheral Blood Mononuclear Cell Oxygen Consumption and Systemic Bioenergetics in Glaucoma Management.International journal of molecular sciences · 2026Review
- Intermittent fasting reduces glaucomatous damage in an HSP27 autoimmune mouse model.Frontiers in cellular neuroscience · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metformin, a first-line treatment for type 2 diabetes, has gained attention as a promising neuroprotective agent due to its pleiotropic effects - including anti-inflammatory, anti-apoptotic, and autophagy-enhancing properties. Here we provide both preclinical and clinical evidence demonstrating the neuroprotective effects of metformin in the context of retinal ganglion cell (RGC) degeneration, a hallmark of glaucoma, a leading cause of irreversible blindness for which no direct RGC-neuroprotective therapies are currently available. In a mouse model of retinal ischemia/reperfusion injury systemic administration of metformin significantly prevented RGC loss and preserved retinal structure. Enhanced phosphorylation of AMP-activated protein kinase (AMPK) was observed, along with increased autophagosome formation and upregulation of key mitophagy markers - including LC3II, optineurin, and Parkin - indicating improved mitochondrial quality control mechanisms. Proteomic analysis revealed that metformin modulated several proteins implicated in mitochondrial respiratory function, ubiquitination, and intracellular trafficking, suggesting broader effects on retinal cellular homeostasis. Complementing our preclinical observations, a retrospective clinical study in diabetic patients with glaucoma showed that individuals treated with metformin maintained stable visual field (VF) parameters over a six-month period, whereas those treated with insulin exhibited significant VF deterioration. These findings position metformin as a promising intraocular pressure (IOP)-independent neurotherapeutic for slowing or preventing glaucomatous neurodegeneration.
Identifiers
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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.