Evidence map›Paper›PMID 28085137›Full record

ArticleEye (London, England)2017

Biomarkers for glaucoma: from the lab to the clinic.

N Von Thun Und Hohenstein-Blaul, S Kunst, N Pfeiffer, F H Grus

Open access · bronzeAbstract read
In one paragraph

Article in Eye (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Glaucoma Animal Models beyond Chronic IOP Increase.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Protein Biomarkers in Glaucoma: A Review.Journal of clinical medicine · 2021
    Review
  14. Review
  15. Article
  16. Synthesis, Characterization, andFrontiers in pharmacology · 2021
    Article
  17. Neuroinflammation as a target for glaucoma therapy.Neural regeneration research · 2019
    Review
  18. Article
  19. Review
  20. Role of Cataract Surgery in the Management of Glaucoma.International ophthalmology clinics · 2018
    Review
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.

N Von Thun Und Hohenstein-BlaulExperimental and Translational Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
S KunstExperimental and Translational Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
N PfeifferExperimental and Translational Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
F H GrusExperimental and Translational Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glaucoma, a leading cause of irreversible blindness worldwide, is often not diagnosed until many years after disease onset. Early and objective diagnostic measures are yet missing. Besides the main risk factor, an elevated intraocular pressure (IOP), age, sex, and ethnicity are known to affect disease progression and severity. Furthermore, oxidative stress, elevated glutamate concentrations, and an autoimmune component are considered possible risk factors. We could identify several potential proteomic biomarkers in glaucoma and examine distinct changes in the glaucomatous human retina proteome. Using an experimental autoimmune glaucoma animal (EAG) model we could demonstrate an IOP-independent loss of retinal ganglion cells (RGC), which is accompanied by antibody depositions and increased levels of microglia. In a different animal model we showed that intermittent IOP elevations provoke neurodegeneration in the optic nerve and the retina and elicit changes of IgG autoantibody reactivities. The correlation between neuronal damage and changes in autoantibody reactivity suggests that autoantibody profiling could be a useful biomarker for glaucoma. In vivo studies on neuroretinal cells and porcine retinal explants demonstrated a protective effect of antibodies (eg, anti-GFAP) on RGC, which seems to be the result of reduced stress levels in the retina. We conclude that the absence of some autoantibodies in glaucoma patients reflects a loss of the protective potential of natural autoimmunity and may thus encourage neurodegenerative processes. Concluding, autoantibody profiles resemble useful biomarkers for diagnosis, progression and severity of glaucoma. Future longitudinal studies will help to improve early detection and enable better monitoring of disease progression.

Indexed as

AnimalsAutoantibodiesAutoimmunityBiomarkersDisease Models, AnimalDisease ProgressionGlaucomaHumansImmunoglobulin GIntraocular PressureMicrogliaProteomicsRetinaRetinal Ganglion CellsSwineAutoantibodiesBiomarkersImmunoglobulin G

Identifiers

PMID28085137
PMCPMC5306474
OpenAlexW2574274573

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.