Evidence map›Paper›PMID 37443787›Full record

ArticleCells2023

Retinal Injury Activates Complement Expression in Müller Cells Leading to Neuroinflammation and Photoreceptor Cell Death.

Steven J Tabor, Kentaro Yuda, Jonathan Deck, Gopalan Gnanaguru, Kip M Connor

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Complement in brain and eye disease: shared mechanisms, convergent pathologies, and common therapeutic opportunities.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
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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

5 authors at 2 institutions in 1 country.

Steven J TaborAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA.
Kentaro YudaAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA.
Jonathan DeckTulane University School of Medicine, Tulane Medical Center, New Orleans, LA 70112, USA.ORCID 0000-0002-7529-1899
Gopalan GnanaguruAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA.
Kip M ConnorAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA.ORCID 0000-0002-2048-9080
Massachusetts Eye and Ear Infirmary · USTulane University · US

Funding

Sex Dependent Regulation of Retinol DegenerationR01EY029269 · NEI · TUFTS MEDICAL CENTER · PI GNANAGURU, GOPALAN · 2019 to 2022
$2.0M
Innate Immunomodulation of Retinal Vascular DevelopmentR01EY032502 · NEI · TUFTS MEDICAL CENTER · PI GNANAGURU, GOPALAN · 2021 to 2024
$1.7M
NEI NIH HHS R01 EY027303ProjectNEI NIH HHS R01 EY029269NEI NIH HHS R01 EY029269ProjectNEI NIH HHS R01 EY032502NEI NIH HHS R01 EY032502Project
6 · The paper itself

Abstract

Retinal detachment (RD) is a neurodegenerative blinding disease caused by plethora of clinical conditions. RD is characterized by the physical separation of retina from the underlying retinal pigment epithelium (RPE), eventually leading to photoreceptor cell death, inflammation, and vision loss. Albeit the activation of complement plays a critical role in the pathogenesis of RD, the retinal cellular source for complement production remains elusive. Here, using C3 tdTomato reporter mice we show that retinal injury upregulates C3 expression, specifically in Müller cells. Activation of the complement cascade results in the generation of proinflammatory cleaved products, C3a and C5a, that bind C3aR and C5aR1, respectively. Our flow cytometry data show that retinal injury significantly upregulated C3aR and C5aR1 in microglia and resulted in the infiltration of peripheral immune cells. Loss of C3, C5, C3aR or C5aR1 reduced photoreceptor cell death and infiltration of microglia and peripheral immune cells into the sub-retinal space. These results indicate that C3/C3aR and C5/C5aR1 play a crucial role in eliciting photoreceptor degeneration and inflammatory responses in RD.

Indexed as

Ependymoglial CellsRetinal DetachmentAnimalsCell DeathComplement System ProteinsMiceNeuroinflammatory DiseasesPhotoreceptor CellsRetinaComplement System ProteinscomplementmicrogliaMüller cellsneurodegenerationneuroinflammationphotoreceptor loss

Identifiers

PMID37443787
PMCPMC10340218
OpenAlexW4382751856

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.