ReviewFrontiers in cell and developmental biology2025
Protein misfolding and mitochondrial dysfunction in glaucoma.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed.
- Neuron-derived SPP1 instructs microglia to limit degeneration.Science advances · 2026Article
- Hydroxysafflor Yellow A for Diabetic Retinopathy: A Critical Review of Retinal Neurovascular Mechanisms and Systemic-to-Ocular Pharmacokinetic Barriers.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial ROS in Retinal Neurodegeneration: Thresholds, Quality Control Failure, and Precision Therapeutic Windows.Biomolecules · 2026Review
- Peripheral Blood Mononuclear Cell Oxygen Consumption and Systemic Bioenergetics in Glaucoma Management.International journal of molecular sciences · 2026Review
- Mitochondria transplantation reduces intraocular pressure by improving mitochondrial function and remodeling trabecular meshwork.Journal of translational medicine · 2026Article
- Disease modeling of myocilin mutation-dependent normal tension glaucoma: human retinal ganglion cell susceptibility to unfolded protein response and mTOR signaling.Stem cells (Dayton, Ohio) · 2026Article
- Article
- Crocin Protects Against Retinal Ischemia-Reperfusion Injury via Regulating Sirt6-Mediated Nrf2/HO-1 Pathway in Rats.Investigative ophthalmology & visual science · 2026Article
- Stage- and compartment-specific remodeling of autophagy and selective mitophagy in glaucoma: from aqueous outflow dysfunction to retinal ganglion cell neurodegeneration.Frontiers in cell and developmental biology · 2026Review
- Pathogenesis of Neovascular Glaucoma in Diabetic Retinopathy: A Review.Journal of ophthalmology · 2026Review
- The key mechanisms and intervention strategies of cell-type-specific mitochondrial metabolism in ophthalmic diseases.Frontiers in cell and developmental biology · 2026Review
- Insights into the molecular mechanism of neurological diseases and their pathophysiological responses.Archives of toxicology · 2025Review
- Single-cell RNA-seq reveals cell type-specific molecular and genetic associations with primary open-angle glaucoma.Signal transduction and targeted therapy · 2025Article
- Establishment of an Advanced In Vitro Model for Pseudoexfoliation Syndrome and Glaucoma.Investigative ophthalmology & visual science · 2025Article
- Beyond the Eye: Glaucoma and the Brain.Brain sciences · 2025Review
- Single-cell profiling of trabecular meshwork identifies mitochondrial dysfunction in a glaucoma model that is protected by vitamin B3 treatment.bioRxiv : the preprint server for biology · 2025Article
- Pyrroloquinoline Quinone (PQQ) Attenuates Hydrogen Peroxide-Induced Injury Through the Enhancement of Mitochondrial Function in Human Trabecular Meshwork Cells.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Glaucoma is a leading cause of irreversible blindness worldwide. Elevated intraocular pressure caused by restricted outflow of the aqueous humor leads to the degeneration of retinal ganglion cells (RGCs) and their axons. Emerging evidence suggests that pathological mechanisms relating to protein folding and mitochondrial dysfunction are significant factors in the disease onset of different types of open-angle glaucoma. In this review, we discuss these defects in three distinct types of open-angle glaucoma: primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and exfoliation glaucoma (XFG). Genetic mutations linked to the previously mentioned open-angle glaucoma, including those in myocilin (MYOC), optineurin (OPTN), and lysyl oxidase 1 (LOXL1), disrupt protein folding and homeostasis, leading to endoplasmic reticulum stress, activation of the unfolded protein response and impaired autophagic protein degradation. These factors contribute to trabecular meshwork and retinal ganglion cell apoptosis. In addition to protein folding defects, mitochondrial dysfunction is also associated with the progression of trabecular meshwork damage and the death of RGCs. Factors such as oxidative stress, an altered mitochondrial fission-fusion balance, and mitophagy dysregulation make RGCs vulnerable and contribute to optic nerve degeneration. The crosstalk between protein folding and mitochondrial defects in glaucoma underscores the complexity of disease pathogenesis and offers potential targets for therapeutic intervention. Strategies aimed at restoring protein homeostasis, enhancing mitochondrial function, and mitigating cellular stress responses hold promise for neuroprotection in glaucoma.
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Registered trials
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