Evidence map›Paper›PMID 25231952›Full record

ArticleGlia2015

Reactive retinal microglia, neuronal survival, and the formation of retinal folds and detachments.

Andy J Fischer, Christopher Zelinka, Nima Milani-Nejad

Open access · bronzeAbstract read
In one paragraph

Article in Glia, 2015. 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
4.0field-weighted citation impact, top 7% 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, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Fibrotic Changes in Rhegmatogenous Retinal Detachment.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Proliferative Vitreoretinopathy: A Reappraisal.Journal of clinical medicine · 2023
    Review
  12. Neuroprotective Effect of α-Lipoic Acid against AβMolecules (Basel, Switzerland) · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Effects of ranibizumab on growth factors and mediators of inflammation in the aqueous humor of patients with diabetic macular edema.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2021
    Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Andy J FischerDepartment of Neuroscience, College of Medicine, The Ohio State University, Columbus, Ohio.
Christopher Zelinka
Nima Milani-Nejad
The Ohio State University · US

Funding

Muller glia: roles in retinal homeostasis and neuronal regenerationR01EY022030 · NEI · OHIO STATE UNIVERSITY · PI FISCHER, ANDY J · 2012 to 2021
$3.5M
NEI NIH HHS EY022030-02NEI NIH HHS R01 EY022030
6 · The paper itself

Abstract

Reactive microglia and macrophages are prevalent in damaged retinas. Accordingly, we investigate how the activation or ablation of microglia/macrophages influences the survival of neurons in the chick retina in vivo. We applied intraocular injections of interleukin 6 (IL6) to stimulate the reactivity of microglia/macrophages and clodronate-liposomes to ablate microglia/macrophages. Activation of the microglia/macrophages with IL6 delays the death of retinal neurons from N-methyl-D-aspartate (NMDA) -induced excitotoxicity. In addition, activation of microglia/macrophages combined with colchicine-mediated retinal damage diminished the survival of ganglion cells. Application of IL6 after an excitotoxic insult greatly exacerbates the damage, and causes widespread retinal detachments and folds, accompanied by accumulation of microglia/macrophages in the subretinal space. Damage-induced retinal folds and detachments were significantly reduced by the ablation of microglia/macrophages. We conclude that microglial reactivity is detrimental to the survival of ganglion cells in colchicine-damaged retinas and detrimental to the survival of photoreceptors in retinal folds. In addition, we conclude that IL6-treatment transiently protects amacrine and bipolar cells against an excitotoxic insult. We propose that suppressing reactivity of microglia/macrophages may be an effective means to lessen the damage and vision loss resulting from damage, in particular during retinal detachment injuries.

Indexed as

Age FactorsAnimalsAnimals, NewbornCell DeathChickensClodronic AcidDisease Models, AnimalExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingInterleukin-6Leukocyte Common AntigensLiposomesMacrophagesMicrogliaNeuronsN-MethylaspartateClodronic AcidExcitatory Amino Acid AgonistsInterleukin-6Leukocyte Common AntigensLiposomesN-MethylaspartatePlant LectinsRicinus communis agglutinin-1Sox9 protein, mouseSOX9 Transcription FactormicrogliaMüller glianeuronal survivalretinaretinal detachment

Identifiers

PMID25231952
PMCPMC4268330
OpenAlexW1613918123

What OpenQuestion holds

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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.