Evidence map›Paper›PMID 27297042›Full record

ArticleScientific reports2016

TLR2/4 deficiency prevents oxygen-induced vascular degeneration and promotes revascularization by downregulating IL-17 in the retina.

Chang He, Peilong Lai, Jing Wang, Tian Zhou, Zijing Huang, Lingli Zhou, Xialin Liu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Current Perspectives of TLR2 Signalling in the Retina.Advances in experimental medicine and biology · 2025
    Review
  4. Article
  5. Ouabain-NaNeurochemical research · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Molecular mechanisms of retinal ischemia.Current opinion in physiology · 2019
    Article
  10. Article
  11. Article
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

7 authors at 2 institutions in 1 country.

Chang HeState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou 510060, P. R. China.
Peilong LaiDepartment of Haematology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, P. R. China.
Jing WangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou 510060, P. R. China.
Tian ZhouState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou 510060, P. R. China.
Zijing HuangState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou 510060, P. R. China.
Lingli ZhouState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou 510060, P. R. China.
Xialin LiuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou 510060, P. R. China.
Sun Yat-sen University · CNGuangdong General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular degeneration is a critical pathological process in many human degenerative diseases, which need efficient ways to revascularization. However, little is known about cellular and molecular mechanisms that are used during vascular degeneration and revascularization. Here, we show that Toll-like receptor 2 and 4 (TLR2/4) double deficiency suppressed hyperoxia induced retinal vessel regression in an oxygen-induced retinopathy (OIR) model. Notably, the TLR2/4-/- mice experienced more revascularization after reduced vessel regression compared with wild-type mice, accompanied with less activation of glial cells. Mechanistically, TLR2/4 activation can tip the balance between Th17 cells and regulatory T cells towards Th17 cells, a critical source of the IL-17A. Less migration and infiltration of IL-17A-expressing proinflammatory cells but elevated regulatory T cells were observed in OIR-retinae from TLR2/4-/- mice. Coincidentally, TLR2/4 deficiency suppressed IL-17A production and increased expressions of anti-inflammatory genes. Furthermore, IL-17A promoted activation of glial cells. IL-17A blockade using a neutralizing antibody alleviated retinal cell apoptosis and glial activation in C57/B6-OIR mice, demonstrating the important role of IL-17A pathway in glial function during revascularization. Thus TLR2/4-mediated IL-17A inflammatory signaling is involved in vessel degeneration and revascularization, indicating that modulation of the TLR2/4-IL-17A pathway may be a novel therapeutic strategy for degenerative diseases.

Indexed as

Down-RegulationNeovascularization, PhysiologicAnimalsCell ProliferationDisease Models, AnimalFemaleGene Expression RegulationInflammationInterleukin-17MaleMice, KnockoutNeurogliaOxygenRetinaRetinal VesselsT-Lymphocytes, RegulatoryInterleukin-17OxygenToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID27297042
PMCPMC4906284
OpenAlexW2423672239

What OpenQuestion holds

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LicenceCC BY
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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.