Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (740 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An ocular disease, occurring in many forms, having as its primary characteristics an unstable or a sustained increase in the intraocular pressure which the eye cannot withstand without damage to its structure or impairment of its function. The consequences of the increased pressure may be manifested in a variety of symptoms, depending upon type and severity, such as excavation of the optic disk, hardness of the eyeball, corneal anesthesia, reduced visual acuity, seeing of colored halos around lights, disturbed dark adaptation, visual field defects, and headaches. (Dictionary of Visual Science, 4th ed)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Glaucomas.
Where it fits in the MeSH classification
- Broader topics
- Ocular Hypertension
- Narrower topics
- Glaucoma, Angle-Closure; Glaucoma, Neovascular; Glaucoma, Open-Angle; Low Tension Glaucoma
- See also
- Sclerostomy; Trabeculectomy; Filtering Surgery; Iridocorneal Endothelial Syndrome
Research landscape
PubMed indexes 65,860 records tagged with the MeSH heading “Glaucoma” (counts retrieved 2026-11-04). 13,201 of them (20.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 24,793 records.
Reviews account for 6,651 records (10.1%) and meta-analyses for 612. Randomized controlled trials number 2,615 (4.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 24,793 |
| 2000-2009 | 11,440 |
| 2010-2019 | 16,426 |
| 2020 onward | 13,201 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 6,651 | 10.1% |
| Meta-analyses | 612 | 0.9% |
| Randomized controlled trials | 2,615 | 4.0% |
Method: PubMed query "Glaucoma"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in eye, ear, nose and throat
Eye, hearing, nose and throat studies rely on specialist tests (visual acuity, eye pressure, audiograms, scopes) and on patient-reported symptoms, which vary between people and with age. Some conditions improve without treatment, so comparison groups matter. Nothing on this page is advice about diagnosis or treatment; sudden loss of sight or hearing needs urgent care from a qualified clinician. Check how the outcome was tested, the age of the people studied and how long they were followed.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Pharmacological restoration of impaired autophagy in retinal ganglion cells prevents abnormal mitochondrial accumulation and glaucomatous neurodegeneration | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 42143320 · DOI · PMC13242679 |
| Mucoadhesive and corneal permeable nano eye drops for improved anti-glaucoma therapy | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41692731 · DOI · PMC12961861 |
| Astrocyte Heterogeneity and Metabolic Reprogramming: Mechanisms Governing Retinal Ganglion Cell Damage in Glaucoma | 2026 | Review article Design not recorded in structured metadata | 2 | cc by PMID 41892278 · DOI · PMC13025485 |
Pharmacological restoration of impaired autophagy in retinal ganglion cells prevents abnormal mitochondrial accumulation and glaucomatous neurodegeneration [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundProgressive loss of retinal ganglion cells (RGCs) and degeneration of optic nerve (ON) axons are the key pathological hallmarks of glaucoma, the leading cause of irreversible blindness.
- Closing excerpt
- Enhancing autophagy in RGCs represents a promising therapeutic strategy to prevent glaucomatous neurodegeneration.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (381 words)
BackgroundProgressive loss of retinal ganglion cells (RGCs) and degeneration of optic nerve (ON) axons are the key pathological hallmarks of glaucoma, the leading cause of irreversible blindness. Elevated intraocular pressure (IOP), primarily due to dysfunction of the trabecular meshwork (TM), remains the most significant and only known modifiable risk factor. However, vision loss persists in some patients despite effective IOP control, highlighting the critical need to elucidate the mechanisms driving glaucomatous neurodegeneration. Emerging evidence links mitochondrial dysfunction to glaucomatous neurodegeneration, yet the precise mechanisms remain poorly defined. Here, we investigate whether defective autophagy/mitophagy, which removes damaged mitochondria, contributes to mitochondrial accumulation, oxidative stress, and neurodegeneration in glaucoma. We further explore the therapeutic potential of enhancing autophagy to improve mitochondrial turnover, mitigate RGC loss, and preserve visual function.MethodsGlucocorticoid (GC)-induced and myocilin (MYOC)-associated glaucoma mouse models were used to assess the expression of mitochondrial markers (TOM20/COX IV), oxidative DNA damage (8-OHdG), and mitophagy/autophagy-related proteins (p62, LC3, Phospho-ubiquitin (Ser65), and LAMP1) in retinal tissues. Transmission electron microscopy (TEM) was employed to analyze mitochondrial accumulation in glaucomatous ON. Mitophagy flux was assessed at early and late stages of neurodegeneration using mitophagy reporter Mt-Keima mice. The effect of RGC-specific autophagy deficiency on mitochondrial accumulation and neurodegeneration was further investigated using Atg5flox/flox mice, in which Atg5 deletion was induced by AAV2-Cre delivery. Additionally, the therapeutic effect of enhancing autophagy with Torin 2 to restore mitochondrial turnover and prevent glaucomatous neurodegeneration was evaluated in both GC-induced and myocilin-associated glaucoma models, as well as in ex vivo human retinal explants.ResultsChronic IOP elevation led to increased mitochondrial accumulation, oxidative DNA damage, and impaired mitophagy/autophagy in glaucomatous retina. TEM analysis further confirmed the accumulation of structurally abnormal mitochondria in glaucomatous ON. In Mt-Keima mice, chronic IOP elevation significantly reduced mitophagy flux prior to RGC loss, indicating that mitophagy impairment precedes neurodegeneration. RGC-specific Atg5 deletion induced the accumulation of damaged mitochondria, leading to neurodegeneration in Atg5 flox/flox mice. Notably, pharmacological restoration of impaired autophagy with Torin 2 prevented mitochondrial accumulation and preserved the structural and functional integrity of RGCs and their axons in glaucoma mouse models and ex vivo human retinal explant cultures.ConclusionOur study indicates impaired autophagy contributes to damaged mitochondrial accumulation and oxidative stress, leading to glaucomatous neurodegeneration. Enhancing autophagy in RGCs represents a promising therapeutic strategy to prevent glaucomatous neurodegeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42143320 · DOI · PMC13242679
Mucoadhesive and corneal permeable nano eye drops for improved anti-glaucoma therapy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Glaucoma, characterized by elevated intraocular pressure (IOP), is the leading cause of irreversible vision loss worldwide.
- Closing excerpt
- Collectively, these findings highlight the potential of natural biopolymer-based nanosystems as efficient eye drop formulations for glaucoma treatment.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (243 words)
Glaucoma, characterized by elevated intraocular pressure (IOP), is the leading cause of irreversible vision loss worldwide. While topical eye drops remain the standard for IOP control, ocular surface dynamic and static barriers significantly limit intraocular drug bioavailability. Enhancing corneal retention and permeability is therefore crucial for effective glaucoma therapy. Here, we developed lignin-based nanoparticles coated with quaternary ammonium chitosan oligosaccharide (Lig-QCOS) for encapsulating and delivering the lipophilic drug latanoprost (Lat), a first-line hypotensive agent. The resulting Lat@Lig-QCOS nanoparticles exhibited a hydrodynamic size of ~ 225.6 nm, a low polydispersity index of 0.08, and a positive Zeta potential of + 21.5 mV. The positively charged surface enables prolonged ocular mucoadhesion and concurrently modulates corneal epithelial tight junctions, enhancing paracellular permeation. This dual mechanism increased corneal permeability by 2.2-fold within 6 h, thereby promoting transcorneal drug transport. In a dexamethasone-induced mouse glaucoma model, a single topical dose of Lat@Lig-QCOS nanoparticles achieved a superior IOP reduction compared to free Lat and anionic Lat@Lig nanoparticles. The formulation produced a maximum IOP reduction of 5.2 mmHg, outperforming the commercial Xalatan® (4.1 mmHg), and sustained efficacy for up to 10 h. The area under the pharmacodynamic response curve (AUC) of Lat@Lig-QCOS was 3.1-fold greater than that of free latanoprost, indicating markedly improved therapeutic performance. Comprehensive in vitro and in vivo biocompatibility assessments confirmed the excellent safety profile of the Lig-QCOS nanocarrier. Collectively, these findings highlight the potential of natural biopolymer-based nanosystems as efficient eye drop formulations for glaucoma treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41692731 · DOI · PMC12961861
Astrocyte Heterogeneity and Metabolic Reprogramming: Mechanisms Governing Retinal Ganglion Cell Damage in Glaucoma [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Glaucoma, a leading cause of irreversible visual impairment, is driven by progressive retinal ganglion cell (RGC) degeneration.
- Closing excerpt
- By unraveling the interplay between astrocyte heterogeneity, metabolic reprogramming, and RGC vulnerability, this review provides novel theoretical frameworks to inform targeted glaucoma therapies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (116 words)
Glaucoma, a leading cause of irreversible visual impairment, is driven by progressive retinal ganglion cell (RGC) degeneration. Emerging evidence highlights astrocytes as pivotal players in its pathogenesis, with their heterogeneity and pathological metabolic reprogramming profoundly impacting RGC survival. This review synthesizes current insights into astrocyte diversity and metabolic alterations during glaucoma-related RGC injury, emphasizing molecular mechanisms from proteomic studies. Key focuses include fatty acid metabolism, neuroinflammation, and signaling pathways that modulate astrocyte function and contribute to neurodegeneration. Despite advances, challenges remain-particularly in characterizing astrocyte subtypes and identifying actionable targets within astrocyte-mediated metabolic/inflammatory cascades. By unraveling the interplay between astrocyte heterogeneity, metabolic reprogramming, and RGC vulnerability, this review provides novel theoretical frameworks to inform targeted glaucoma therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41892278 · DOI · PMC13025485
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis [4]
- Research article The Complications of Myopia: A Review and Meta-Analysis [5]
- Research article Myopia as a risk factor for open-angle glaucoma: a systematic review and meta-analysis [6]
- Research article Genome-wide meta-analysis identifies 127 open-angle glaucoma loci with consistent effect across ancestries [7]
- Research article Minimally-invasive glaucoma surgeries (MIGS) for open angle glaucoma: A systematic review and meta-analysis [8]
- Research article Comparative Effectiveness of First-Line Medications for Primary Open-Angle Glaucoma: A Systematic Review and Network Meta-analysis [9]
References
- Maddineni P, Kaipa BR, Kodati B, Kesavan K, Li L, Millar JC, et al.. Pharmacological restoration of impaired autophagy in retinal ganglion cells prevents abnormal mitochondrial accumulation and glaucomatous neurodegeneration. . 2026. PMID 42143320 · DOI · PMC13242679
- Zhang X, Shao Q, Yu M, Huang Y, Wang Y, Wen Y, et al.. Mucoadhesive and corneal permeable nano eye drops for improved anti-glaucoma therapy. . 2026. PMID 41692731 · DOI · PMC12961861
- Hao Y, Liang D, Ren M, Kuang F, Wu M. Astrocyte Heterogeneity and Metabolic Reprogramming: Mechanisms Governing Retinal Ganglion Cell Damage in Glaucoma. . 2026. PMID 41892278 · DOI · PMC13025485
- Tham YC, Li X, Wong TY, Quigley HA, Aung T, Cheng CY. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology. 2014. PMID 24974815 · DOI
- Haarman AEG, Enthoven CA, Tideman JWL, Tedja MS, Verhoeven VJM, Klaver CCW. The Complications of Myopia: A Review and Meta-Analysis. Invest Ophthalmol Vis Sci. 2020. PMID 32347918 · DOI · PMC7401976
- Marcus MW, de Vries MM, Junoy Montolio FG, Jansonius NM. Myopia as a risk factor for open-angle glaucoma: a systematic review and meta-analysis. Ophthalmology. 2011. PMID 21684603 · DOI
- Gharahkhani P, Jorgenson E, Hysi P, Khawaja AP, Pendergrass S, Han X, et al.. Genome-wide meta-analysis identifies 127 open-angle glaucoma loci with consistent effect across ancestries. Nat Commun. 2021. PMID 33627673 · DOI · PMC7904932
- Lavia C, Dallorto L, Maule M, Ceccarelli M, Fea AM. Minimally-invasive glaucoma surgeries (MIGS) for open angle glaucoma: A systematic review and meta-analysis. PLoS One. 2017. PMID 28850575 · DOI · PMC5574616
- Li T, Lindsley K, Rouse B, Hong H, Shi Q, Friedman DS, et al.. Comparative Effectiveness of First-Line Medications for Primary Open-Angle Glaucoma: A Systematic Review and Network Meta-analysis. Ophthalmology. 2016. PMID 26526633 · DOI · PMC4695285
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.