Evidence map›Paper›PMID 30651837›Full record

ReviewExperimental and therapeutic medicine2019

Normal-tension glaucoma: Pathogenesis and genetics.

Alexandra Trivli, Ioannis Koliarakis, Chryssa Terzidou, George N Goulielmos, Charalambos S Siganos, Demetrios A Spandidos, Georgios Dalianis, Efstathios T Detorakis

Open access · diamondAbstract readReview
In one paragraph

Review in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
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  13. Observational
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  18. Glaucoma Animal Models beyond Chronic IOP Increase.International journal of molecular sciences · 2024
    Review
  19. Article
  20. Review

3 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

8 authors at 3 institutions in 1 country.

Alexandra TrivliDepartment of Ophthalmology, Konstantopouleio-Patission General Hospital, 14233 Athens, Greece.
Ioannis KoliarakisLaboratory of Anatomy-Histology-Embryology, Medical School, University of Crete, 71003 Heraklion, Greece.
Chryssa TerzidouDepartment of Ophthalmology, Konstantopouleio-Patission General Hospital, 14233 Athens, Greece.
George N GoulielmosSection of Molecular Pathology and Human Genetics, Department of Internal Medicine, School of Medicine, University of Crete, 71003 Heraklion, Greece.
Charalambos S SiganosDepartment of Ophthalmology, University Hospital of Heraklion, 71110 Heraklion, Greece.
Demetrios A SpandidosLaboratory of Clinical Virology, Medical School, University of Crete, 71003 Heraklion, Greece.
Georgios DalianisDepartment of Ophthalmology, Konstantopouleio-Patission General Hospital, 14233 Athens, Greece.
Efstathios T DetorakisDepartment of Ophthalmology, University Hospital of Heraklion, 71110 Heraklion, Greece.
Agia Olga Hospital · GRUniversity of Crete · GRUniversity Hospital of Heraklion · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Normal-tension glaucoma (NTG) is a multifactorial optic neuropathy which, similar to open-angle glaucomas, is characterized by progressive retinal ganglion cell death and glaucomatous visual field loss. The major distinction of NTG from open-angle glaucomas is that the intraocular pressure (IOP) does not exceed the normal range. Missing the major risk factor and target of therapy, the elevated IOP, NTG poses a clinical challenge. Several insightful reviews have been published on the pathophysiology of NTG describing the possible underlying mechanisms. The current literature available also suggests that a significant percentage of patients with NTG (as high as 21%) have a family history of glaucoma, indicating a genetic predisposition to the disease. These facts strengthen the indication that NTG remains an enigmatic process. The aim of this review was to summarize the vascular, mechanical and genetic components considered to be responsible for NTG development and to discuss the mechanisms through which they are involved in the pathogenesis of NTG.

Indexed as

geneticsglaucomaintraocular pressurenormal tensionpathogenesis

Identifiers

PMID30651837
PMCPMC6307418
OpenAlexW2903318616

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.