Evidence map›Paper›PMID 29290065›Full record

ReviewInternational ophthalmology2019

Pathophysiology of primary open-angle glaucoma from a neuroinflammatory and neurotoxicity perspective: a review of the literature.

Karine Evangelho, Maria Mogilevskaya, Monica Losada-Barragan, Jeinny Karina Vargas-Sanchez

Abstract readReview
PubMed Publisher
In one paragraph

Review in International ophthalmology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 3 pooled it
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 3 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Metabolomics in Glaucoma: A Systematic Review.Investigative ophthalmology & visual science · 2021
    Pooled it
  4. Trial
  5. Trial
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Considerations and implications of currentFrontiers in cell and developmental biology · 2025
    Review
  17. Review
  18. Article
  19. Article
  20. Article

22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Karine EvangelhoGrupo de Investigación en Ciencias Biomédicas GRINCIBIO, Facultad de medicina, Sede Bogotá, Universidad Antonio Nariño, Bogotá, Colombia.
Maria MogilevskayaGrupo de Investigación en Ingeniería Clínica - Hospital Universitario la Samaritana GINIC-HUS, Sede Bogotá, ECCI, Bogotá, Colombia.
Monica Losada-BarraganGrupo de Biología Celular y Funcional e Ingeniería de Biomoléculas, Facultad de Ciencias, Sede Bogotá, Universidad Antonio Nariño, Bogotá, Colombia.
Jeinny Karina Vargas-SanchezGrupo de Investigación en Ciencias Biomédicas GRINCIBIO, Facultad de medicina, Sede Bogotá, Universidad Antonio Nariño, Bogotá, Colombia. jeinny.vargas@uan.edu.co.
Universidad Antonio Nariño · COHospital Universitario de la Samaritana · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGlaucoma is the leading cause of blindness in humans, affecting 2% of the population. This disorder can be classified into various types including primary, secondary, glaucoma with angle closure and with open angle. The prevalence of distinct types of glaucoma differs for each particular region of the world. One of the most common types of this disease is primary open-angle glaucoma (POAG), which is a complex inherited disorder characterized by progressive retinal ganglion cell death, optic nerve head excavation and visual field loss. Nowadays, POAG is considered an optic neuropathy, while intraocular pressure is proposed to play a fundamental role in its pathophysiology and especially in optic disk damage. However, the exact mechanism of optic nerve head damage remains a topic of debate. This literature review aims to bring together the information on the pathophysiology of primary open-angle glaucoma, particularly focusing on neuroinflammatory mechanisms leading to the death of the retinal ganglion cell.

methodsA literature search was done on PubMed using key words including primary open-angle glaucoma, retinal ganglion cells, Müller cells, glutamate, glial cells, ischemia, hypoxia, exitotoxicity, neuroinflammation, axotomy and neurotrophic factors. The literature was reviewed to collect the information published about the pathophysiologic mechanisms of RGC death in the POAG, from a neuroinflammatory and neurotoxicity perspective.

resultsProposed mechanisms for glaucomatous damage are a result of pressure in RGC followed by ischemia, hypoxia of the ONH, and consequently death due to glutamate-induced excitotoxicity, deprivation of energy and oxygen, increase in levels of inflammatory mediators and alteration of trophic factors flow. These events lead to blockage of anterograde and retrograde axonal transport with ensuing axotomy and eventually blindness.

conclusionsThe damage to ganglion cells and eventually glaucomatous injury can occur via various mechanisms including baric trauma, ischemia and impact of metabolic toxins, which triggers an inflammatory process and secondary degeneration in the ONH.

Indexed as

Glaucoma, Open-AngleHumansIntraocular PressureOptic DiskOptic Nerve DiseasesRetinal Ganglion CellsVision DisordersVisual FieldsCell deathGlaucomaGlutamateIntraocular pressureNeuroinflammationRetinal ganglion cells

Identifiers

PMID29290065
OpenAlexW2777517651

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.