Evidence map›Paper›PMID 38110030›Full record

ReviewProgress in retinal and eye research2024

IOP and glaucoma damage: The essential role of optic nerve head and retinal mechanosensors.

Ian Pitha, Liya Du, Thao D Nguyen, Harry Quigley

Open access · greenAbstract readReview
In one paragraph

Review in Progress in retinal and eye research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
13.1field-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

42 citing papers in PubMed, 47 citations in OpenAlex.

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  15. Vascular regeneration and blood flow recovery in glaucoma.Frontiers in cell and developmental biology · 2026
    Review
  16. Article
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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 1 institution in 1 country.

Ian PithaDepartment of Ophthalmology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Center for Nanomedicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Glaucoma Center of Excellence, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Liya DuDepartment of Ophthalmology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Thao D NguyenDepartment of Ophthalmology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Mechanical Engineering, The Johns Hopkins University, Baltimore, MD, USA.
Harry QuigleyDepartment of Ophthalmology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Glaucoma Center of Excellence, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: hquigley@jhmi.edu.
Johns Hopkins University · US

Funding

Wilmer Core Grant for Vision ResearchP30EY001765 · NEI · JOHNS HOPKINS UNIVERSITY · PI JEFFREY MUMM · 1985 to 2026
$22.1M
PATHOGENESIS OF GLAUCOMATOUS OPTIC NERVE DAMAGER01EY002120 · NEI · JOHNS HOPKINS UNIVERSITY · PI QUIGLEY, HARRY ALAN · 1985 to 2025
$12.6M
NEI NIH HHS P30 EY001765NEI NIH HHS R01 EY002120
6 · The paper itself

Abstract

There are many unanswered questions on the relation of intraocular pressure to glaucoma development and progression. IOP itself cannot be distilled to a single, unifying value, because IOP level varies over time, differs depending on ocular location, and can be affected by method of measurement. Ultimately, IOP level creates mechanical strain that affects axonal function at the optic nerve head which causes local extracellular matrix remodeling and retinal ganglion cell death - hallmarks of glaucoma and the cause of glaucomatous vision loss. Extracellular tissue strain at the ONH and lamina cribrosa is regionally variable and differs in magnitude and location between healthy and glaucomatous eyes. The ultimate targets of IOP-induced tissue strain in glaucoma are retinal ganglion cell axons at the optic nerve head and the cells that support axonal function (astrocytes, the neurovascular unit, microglia, and fibroblasts). These cells sense tissue strain through a series of signals that originate at the cell membrane and alter cytoskeletal organization, migration, differentiation, gene transcription, and proliferation. The proteins that translate mechanical stimuli into molecular signals act as band-pass filters - sensing some stimuli while ignoring others - and cellular responses to stimuli can differ based on cell type and differentiation state. Therefore, to fully understand the IOP signals that are relevant to glaucoma, it is necessary to understand the ultimate cellular targets of IOP-induced mechanical stimuli and their ability to sense, ignore, and translate these signals into cellular actions.

Indexed as

GlaucomaOptic DiskAxonsHumansIntraocular PressureRetinal Ganglion Cells

Identifiers

PMID38110030
PMCPMC10960268
OpenAlexW4389849227

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.