ArticleeLife2023
Metformin protects trabecular meshwork against oxidative injury via activating integrin/ROCK signals.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Protective Role of Metformin in Glaucoma: Prospective Cohort Study, Meta-Analysis, and Drug-Target Mendelian Randomization.Ophthalmology science · 2026Article
- Peripheral Blood Mononuclear Cell Oxygen Consumption and Systemic Bioenergetics in Glaucoma Management.International journal of molecular sciences · 2026Review
- The role of metformin in extracellular matrix-based three-dimensional cell culture Models: A mini-review on therapeutic potentials.Biochemistry and biophysics reports · 2026Review
- Glaucoma Risk with Metformin and Sulfonylurea Therapies in Type 2 Diabetes: A Retrospective Cohort Study.Clinical ophthalmology (Auckland, N.Z.) · 2026Article
- Review
- Neuroprotective Effects of Metformin on Cerebral Ischemia-Reperfusion Injury: Modulation of JNK and p38 MAP Kinase Signaling Pathways.Cell biochemistry and biophysics · 2024Article
- Steroid-Induced Ocular Hypertension in Mice Is Differentially Reduced by Selective EP2, EP3, EP4, and IP Prostanoid Receptor Agonists.International journal of molecular sciences · 2024Article
- Nutritional Factors: Benefits in Glaucoma and Ophthalmologic Pathologies.Life (Basel, Switzerland) · 2023Review
- Metformin Alleviates Fibrosis of Trabecular Meshwork Cells Induced by TGFβ2 Through the Activation of Autophagy.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the protective effect of metformin on trabecular meshwork (TM) and explore its molecular mechanisms in vivo and in vitro. Ocular hypertension (OHT) mouse models were induced with dexamethasone and further treated with metformin to determine the intraocular pressure (IOP)-lowering effect. Cultured human TM cells (HTMCs) were pre-stimulated with tert-butyl hydroperoxide (tBHP) to induce oxidative damage and then supplemented with metformin for another 24 hr. The expression of fibrotic markers and integrin/Rho-associated kinase (ROCK) signals, including α-smooth muscle actin (α-SMA), transforming growth factor-β (TGF-β), fibronectin, integrin beta 1, ROCK 1/2, AMP-activated protein kinase, myosin light chain 1, and F-actin were determined by western blotting and immunofluorescence. Reactive oxygen species (ROS) content was analysed using flow cytometry. Transmission electron microscopy was performed to observe microfilaments in HTMCs. It showed that metformin administration reduced the elevated IOP and alleviated the fibrotic activity of aqueous humour outflow in OHT models. Additionally, metformin rearranged the disordered cytoskeleton in the TM both in vivo and in vitro and significantly inhibited ROS production and activated integrin/ROCK signalling induced by tBHP in HTMCs. These results indicated that metformin reduced the elevated IOP in steroid-induced OHT mouse models and exerted its protective effects against oxidative injury by regulating cytoskeleton remodelling through the integrin/ROCK pathway. This study provides new insights into metformin use and preclinical evidence for the potential treatment of primary open-angle glaucoma.
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Registered trials
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