Evidence map›Paper›PMID 40374644›Full record

ArticleScientific reports2025

TLR4 deficiency does not alter glaucomatous progression in a mouse model of chronic glaucoma.

Chi Zhang, Marina Simón, Jeffrey M Harder, Haeyn Lim, Christa Montgomery, Qing Wang, Simon W M John

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Chi ZhangDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.
Marina SimónDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.
Jeffrey M HarderThe Jackson Laboratory, Bar Harbor, ME, USA.
Haeyn LimDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.
Christa MontgomeryDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.
Qing WangDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.
Simon W M JohnDepartment of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA. sj2967@cumc.columbia.edu.

Funding

Instrumentation, Fabrication, and Design CoreP30EY019007 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Xin Zhang · 2010 to 2026
$12.9M
Factors Determining Intraocular Pressure and Glaucoma SusceptibilityR01EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 2002 to 2018
$12.4M
Cell Death Pathways in Glaucomatous NeurodegenerationR01EY018606 · NEI · UNIVERSITY OF ROCHESTER · PI JOHN, SIMON W, LIBBY, RICHARD T · 2008 to 2023
$5.8M
Does VECAD at Schlemm canal cell-junctions determine IOP and glaucoma risk?R01EY032062 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI JOHN, SIMON W, KIZHATIL, KRISHNAKUMAR · 2021 to 2025
$3.5M
Models, mechanisms and treatment of LMX1B-induced glaucomaR01EY032507 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI JOHN, SIMON W · 2021 to 2024
$2.3M
FACTORS DETERMINING INTRAOCULAR PRESSURER29EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 1997 to 2001
$227k
NEI NIH HHS EY11721, EY032507, EY032062, EY018606, P30EY019007NEI NIH HHS P30 EY019007NEI NIH HHS R01 EY011721NEI NIH HHS R01 EY018606NEI NIH HHS R01 EY032062NEI NIH HHS R01 EY032507NEI NIH HHS R29 EY011721New York Fund for Innovation in Research and Scientific Talent EMPIRE CU19-2660
6 · The paper itself

Abstract

Glaucoma is a leading cause of irreversible blindness worldwide. Toll-like receptor 4 (TLR4) is a pattern-recognition transmembrane receptor that induces neuroinflammatory processes in response to injury. Tlr4 is highly expressed in ocular tissues and is known to modulate inflammatory processes in both anterior and posterior segment tissues. TLR4 activation can lead to mitochondrial dysfunction and metabolic deficits in inflammatory disorders. Due to its effects on inflammation and metabolism, TLR4 is a candidate to participate in glaucoma pathogenesis. It has been suggested as a therapeutic target based on studies using acute models, such as experimentally raising IOP to ischemia-inducing levels. Nevertheless, its role in chronic glaucoma needs further evaluation. In the current study, we investigated the role of TLR4 in an inherited mouse model of chronic glaucoma, DBA/2J. To do this, we analyzed the effect of Tlr4 knockout (Tlr4

Indexed as

GlaucomaToll-Like Receptor 4AnimalsChronic DiseaseDisease Models, AnimalDisease ProgressionIntraocular PressureMaleMiceMice, Inbred DBAMice, KnockoutTlr4 protein, mouseToll-Like Receptor 4GlaucomaIntraocular pressure (IOP)NeurodegenerationNeuroinflammationToll-like receptor 4 (TLR4)

Identifiers

PMID40374644
PMCPMC12081889

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Registered trials

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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.