Evidence map›Paper›PMID 20708001›Full record

ReviewExperimental eye research2011

Glaucomatous cupping of the lamina cribrosa: a review of the evidence for active progressive remodeling as a mechanism.

J Crawford Downs, Michael D Roberts, Ian A Sigal

Abstract readReview
In one paragraph

Review in Experimental eye research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
8.8field-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

110 citing papers in PubMed, 228 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Primary Cilia of Astrocytes in the Retina in Development and Disease.Investigative ophthalmology & visual science · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Two-Photon Fabrication of Donor-Specific Human Lamina Cribrosa Models.Translational vision science & technology · 2025
    Article
  11. Article
  12. Pericytes in the optic nerve head.Progress in retinal and eye research · 2025
    Review
  13. Article
  14. Role of Microglia in Glaucomatous Pathology.Advances in experimental medicine and biology · 2025
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

50 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

3 authors at 1 institution in 1 country.

J Crawford DownsOcular Biomechanics Laboratory of the Devers Eye Institute, Legacy Health, 1225 NE 2nd Ave., Portland, OR 97232, USA. cdowns@deverseye.org
Michael D Roberts
Ian A Sigal
Legacy Health · US

Funding

Age-related changes in optic nerve head structure and biomechanicsR01EY018926 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DOWNS, J CRAWFORD, GIRKIN, CHRISTOPHER ANTHONY · 2008 to 2015
$2.6M
Racial Variations in Optic Nerve Head Structure and BiomechanicsR01EY019333 · NEI · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI DOWNS, J CRAWFORD, GIRKIN, CHRISTOPHER ANTHONY · 2009 to 2011
$917k
NEI NIH HHS R01 EY018926NEI NIH HHS R01 EY019333NEI NIH HHS R01-EY18926NEI NIH HHS R01-EY19333
6 · The paper itself

Abstract

The purpose of this review is to examine the literature in an attempt to elucidate a biomechanical basis for glaucomatous cupping. In particular, this work focuses on the role of biomechanics in driving connective tissue remodeling in the progression of laminar morphology from a normal state to that of an excavated glaucomatous state. While there are multiple contributing factors to the pathogenesis of glaucoma, we focus on laminar extracellular matrix (ECM) remodeling in glaucoma and the feedback mechanisms and signals that may guide progressive laminar cupping. We review the literature on the potential mechanisms of glaucomatous changes in the laminar ECM at the anatomic, structural, cellular and subcellular levels in the context of the biomechanical paradigm of glaucomatous onset and progression. Several conclusions can be drawn from this review. First, extensive remodeling of the lamina cribrosa ECM occurs in primary open angle glaucoma. Second, there is surprisingly little evidence to support acute mechanical damage to the lamina as the principal mechanism of cupping. Third, ONH astrocytes and lamina cribrosa cells can sense their mechanical environment and respond to mechanical stimuli by remodeling the ECM. Fourth, there is evidence suggesting that chronic remodeling of the lamina results in a progressive posterior migration of the laminar insertion into the canal wall, which eventually results in the posterior lamina inserting into the pia mater. Finally, modeling studies suggest that laminar remodeling may be a biomechanical feedback mechanism through which cells modify their environment in an attempt to return to a homeostatic mechanical environment. It is plausible that biomechanics-driven connective tissue remodeling is a mechanism in the progression of laminar morphology from a normal state to that of a cupped, excavated glaucomatous state.

Indexed as

AnimalsAstrocytesAxonsBiomechanical PhenomenaConnective TissueExtracellular MatrixGlaucoma, Open-AngleHumansIntraocular PressureOptic DiskOptic Nerve DiseasesRetinal Ganglion Cells

Identifiers

PMID20708001
PMCPMC3026919
OpenAlexW2060387702

What OpenQuestion holds

Textmetadata
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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.