Evidence map›Paper›PMID 22262082›Full record

ReviewCurrent opinion in ophthalmology2012

Current understanding of conventional outflow dysfunction in glaucoma.

W Daniel Stamer, Ted S Acott

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in ophthalmology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
237citing papers in PubMed, 1 pooled it
15.2field-weighted citation impact, top 1% 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

237 citing papers in PubMed, 1 synthesis or guideline pooled it, 325 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Acute intraocular pressure changes during isometric exercise in glaucoma patients: the influence of exercise and intensity.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
    Article
  17. Article
  18. Article
  19. Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026
    Review
  20. Article

177 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

2 authors at 2 institutions in 1 country.

W Daniel StamerDepartment of Ophthalmology, Duke University, Durham, North Carolina 27710, USA. dan.stamer@duke.edu
Ted S Acott
Duke University · USOregon Health & Science University · US

Funding

Proteomics CoreP30EY010572 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI TED S ACOTT · 1995 to 2026
$19.4M
BIOLOGY OF TRABECULAR RESPONSE TO LASER TRABECULOPLASTYR01EY008247 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ACOTT, TED S · 1989 to 2017
$7.7M
The Mechanical Basis of Primary Open Angle GlaucomaR01EY019696 · NEI · NORTHWESTERN UNIVERSITY · PI FREDBERG, JEFFREY J, JOHNSON, MARK · 2009 to 2019
$7.6M
eNOS-Dependent Mechanoregulation of Intraocular PressureR01EY022359 · NEI · DUKE UNIVERSITY · PI STAMER, W DANIEL · 2012 to 2025
$5.6M
VERTEBRATE EYE: STUDIES OF AQUEOUS OUTFLOWR01EY003279 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ACOTT, TED S · 1985 to 2012
$5.5M
MOLECULAR BASIS OF MYOCILIN FUNCTION IN THE HUMAN EYER01EY012797 · NEI · UNIVERSITY OF ARIZONA · PI STAMER, W DANIEL · 2001 to 2010
$2.2M
CADHERIN DYNAMICS AND GLAUCOMAR01EY017007 · NEI · UNIVERSITY OF ARIZONA · PI STAMER, W DANIEL · 2006 to 2010
$1.7M
NEI NIH HHS EY003279NEI NIH HHS EY008247NEI NIH HHS EY010572NEI NIH HHS EY017007NEI NIH HHS EY019696NEI NIH HHS P30 EY010572NEI NIH HHS R01 EY003279NEI NIH HHS R01 EY008247NEI NIH HHS R01 EY012797NEI NIH HHS R01 EY019696NEI NIH HHS R01 EY022359
6 · The paper itself

Abstract

purpose of reviewRegulation of intraocular pressure by the conventional (trabecular) outflow pathway is complicated, involving a myriad of mechanical and chemical signals. In most, intraocular pressure is maintained within a tight range over a lifetime. Unfortunately in some, dysfunction results in ocular hypertension and open-angle glaucoma. In the context of established knowledge, this review summarizes recent investigations of conventional outflow function, with the goal of identifying areas for future inquiry and therapeutic targeting. RECENT

findingsMechanical stimulation of conventional outflow cells due to intraocular pressure fluctuations impacts contractility, gene expression, pore formation, enzyme activity, and signaling. Numerous local signaling mediators in the conventional pathway such as bioactive lipids, cytokines, nitric oxide, and nucleotides participate in the regulation of outflow. Interestingly outflow through the conventional pathway is not uniform, but segmental, with passageways constantly changing due to focal protease activity of trabecular cells clearing extracellular matrix materials. The relationship between extracellular matrix expression and trabecular meshwork contractility appears to coordinately impact outflow resistance and is the target of a new class of drugs, the Rho kinase inhibitors. SUMMARY: The conventional outflow pathway is a dynamic, pressure-sensitive tissue that is vulnerable to pathology on many fronts, each representing a therapeutic opportunity.

Indexed as

Aqueous HumorGlaucoma, Open-AngleHumansIntraocular PressureOcular HypertensionSignal TransductionTrabecular Meshwork

Identifiers

PMID22262082
PMCPMC3770936
OpenAlexW2037652817

What OpenQuestion holds

Textmetadata
LicenceTDM
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.