Evidence map›Paper›PMID 27229292›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Pro-fibrotic pathway activation in trabecular meshwork and lamina cribrosa is the main driving force of glaucoma.

Alex Zhavoronkov, Evgeny Izumchenko, Riya R Kanherkar, Mahder Teka, Charles Cantor, Kebreten Manaye, David Sidransky, Michael D West, Eugene Makarev, Antonei Benjamin Csoka

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Wound Modulations in Glaucoma Surgery: A Systematic Review.Bioengineering (Basel, Switzerland) · 2024
    Review
  15. Applications of artificial intelligence and bioinformatics methodologies in the analysis of ocular biofluid markers: a scoping review.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024
    Article
  16. Circadian rhythm of intraocular pressure.The journal of physiological sciences : JPS · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 2 countries.

Alex Zhavoronkova Insilico Medicine, Inc., ETC, Johns Hopkins University , Baltimore , MD , USA.
Evgeny Izumchenkoe Johns Hopkins University , Department of Otolaryngology-Head and Neck Surgery.
Riya R Kanherkarc Vision Genomics, LLC , Washington, DC , USA.
Mahder Tekac Vision Genomics, LLC , Washington, DC , USA.
Charles Cantorf Boston University , Boston , MA , USA.
Kebreten Manayed Epigenetics Laboratory, Howard University , Washington, DC , USA.
David Sidranskyc Vision Genomics, LLC , Washington, DC , USA.
Michael D Westh BioTime, Inc. , Alameda , CA , USA.
Eugene Makareva Insilico Medicine, Inc., ETC, Johns Hopkins University , Baltimore , MD , USA.
Antonei Benjamin Csokac Vision Genomics, LLC , Washington, DC , USA.
Howard University · USJohns Hopkins University · USLineage Cell Therapeutics (United States) · USRetrotope (United States) · USUrology Foundation · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While primary open-angle glaucoma (POAG) is a leading cause of blindness worldwide, it still does not have a clear mechanism that can explain all clinical cases of the disease. Elevated IOP is associated with increased accumulation of extracellular matrix (ECM) proteins in the trabecular meshwork (TM) that prevents normal outflow of aqueous humor (AH) and has damaging effects on the fine mesh-like lamina cribrosa (LC) through which the optic nerve fibers pass. Applying a pathway analysis algorithm, we discovered that an elevated level of TGFβ observed in glaucoma-affected tissues could lead to pro-fibrotic pathway activation in TM and in LC. In turn, activated pro-fibrotic pathways lead to ECM remodeling in TM and LC, making TM less efficient in AH drainage and making LC more susceptible to damage from elevated IOP via ECM transformation in LC. We propose pathway targets for potential therapeutic interventions to delay or avoid fibrosis initiation in TM and LC tissues.

Indexed as

Aqueous HumorComputational BiologyDatasets as TopicExtracellular Matrix ProteinsFibrosisGene Expression ProfilingGene Expression RegulationGene OntologyGlaucoma, Open-AngleHumansIntraocular PressureMicroarray AnalysisMolecular Sequence AnnotationMolecular Targeted TherapyOptic NerveScleraExtracellular Matrix ProteinsTransforming Growth Factor betafibrosisglaucomalamina cribrosaPOAGTGFβtrabecular meshwork

Identifiers

PMID27229292
PMCPMC4934076
OpenAlexW2395451099

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.