Evidence map›Paper›PMID 30666961›Full record

ArticleeLife2019

Absence of TGFβ signaling in retinal microglia induces retinal degeneration and exacerbates choroidal neovascularization.

Wenxin Ma, Sean M Silverman, Lian Zhao, Rafael Villasmil, Maria M Campos, Juan Amaral, Wai T Wong

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  3. Observational
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  14. Article
  15. Article
  16. Article
  17. Inflammation and retinal degenerative diseases.Neural regeneration research · 2023
    Review
  18. International journal of ophthalmology · 2023
    Article
  19. Review
  20. Article

5 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

7 authors at 1 institution in 1 country.

Wenxin MaUnit on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, United States.ORCID 0000-0001-8396-6625
Sean M SilvermanUnit on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, United States.
Lian ZhaoUnit on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, United States.ORCID 0000-0002-0120-1969
Rafael VillasmilFlow Cytometry Core Facility, National Eye Institute, National Institutes of Health, Bethesda, United States.
Maria M CamposSection on Histopathology, National Eye Institute, National Institutes of Health, Bethesda, United States.
Juan AmaralUnit on Ocular Stem Cell and Translational Research, National Eye Institute, National Institutes of Health, Bethesda, United States.
Wai T WongUnit on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, United States.ORCID 0000-0003-0681-4016
National Institutes of Health · US

Funding

Histopathology CoreZICEY000461 · NEI · NATIONAL EYE INSTITUTE · PI SCHNEEWEIS, DAVID · 2009 to 2022
$7.7M
Role of Microglia in the Retina in Retinal DiseasesZIAEY000541 · NEI · NATIONAL EYE INSTITUTE · PI WONG, WAI · 2014 to 2020
$5.2M
NEI NIH HHS Intramural Research Program
6 · The paper itself

Abstract

Constitutive TGFβ signaling is important in maintaining retinal neurons and blood vessels and is a factor contributing to the risk for age-related macular degeneration (AMD), a retinal disease involving neurodegeneration and microglial activation. How TGFβ signaling to microglia influences pathological retinal neuroinflammation is unclear. We discovered that ablation of the TGFβ receptor, TGFBR2, in retinal microglia of adult mice induced abnormal microglial numbers, distribution, morphology, and activation status, and promoted a pathological microglial gene expression profile. TGFBR2-deficient retinal microglia induced secondary gliotic changes in Müller cells, neuronal apoptosis, and decreased light-evoked retinal function reflecting abnormal synaptic transmission. While retinal vasculature was unaffected, TGFBR2-deficient microglia demonstrated exaggerated responses to laser-induced injury that was associated with increased choroidal neovascularization, a hallmark of advanced exudative AMD. These findings demonstrate that deficiencies in TGFβ-mediated microglial regulation can drive neuroinflammatory contributions to AMD-related neurodegeneration and neovascularization, highlighting TGFβ signaling as a potential therapeutic target.

Indexed as

AnimalsApoptosisChoroidal NeovascularizationEpendymoglial CellsMacular DegenerationMice, KnockoutMice, TransgenicMicrogliaReceptor, Transforming Growth Factor-beta Type IIRetinaRetinal DegenerationSignal TransductionSynaptic TransmissionTransforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor betaage-related macular degenerationimmunologyinflammationmicrogliamouseneovascularizationneurodegenerationneuroscienceretinaTGF

Identifiers

PMID30666961
PMCPMC6342522
OpenAlexW2909426653

What OpenQuestion holds

Textmetadata
LicenceCC0
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.