Evidence map›Paper›PMID 33059704›Full record

ArticleJournal of neuroinflammation2020

Cyclooxygenase-1 mediates neuroinflammation and neurotoxicity in a mouse model of retinitis pigmentosa.

Wei Yang, Guoyin Xiong, Bin Lin

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Understanding TAK1 deficiency in microglia: Dual mechanisms for photoreceptor protection in a mouse model of retinitis pigmentosa.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Molecules (Basel, Switzerland) · 2023
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
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 2 institutions in 2 countries.

Wei YangSchool of Optometry, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong.
Guoyin XiongDepartment of Ophthalmology, University of Hong Kong, Pokfulam, Hong Kong.
Bin LinSchool of Optometry, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong. b.lin@polyu.edu.hk.ORCID http://orcid.org/0000-0003-1309-3480
Hong Kong Polytechnic University · HKQueen Mary Hospital · CN

Funding

Health and Medical Research Fund 02132246
6 · The paper itself

Abstract

backgroundRetinitis pigmentosa (RP) is a group of inherited eye disorders with progressive degeneration of photoreceptors in the retina, ultimately leading to partial or complete blindness. The mechanisms underlying photoreceptor degeneration are not yet completely understood. Neuroinflammation is reported to play a pathological role in RP. However, the mechanisms that trigger neuroinflammation remain largely unknown. To address this question, we investigated the role of cyclooxygenase-1 (COX-1), a key enzyme in the conversion of arachidonic acid to proinflammatory prostaglandins, in the rd10 mouse model of RP.

methodsWe backcrossed COX-1 knockout mice (COX-1

resultsWe found that genetic ablation or pharmacological inhibition of COX-1 alleviated neuroinflammation and subsequently preserved retinal photoreceptor and function and visual performance in rd10 mice. Moreover, we observed that the pharmacological inhibition of the prostaglandin E2 (PGE2) EP2 receptors largely replicated the beneficial effects of COX-1 deletion, suggesting that EP2 receptor was a critical downstream effector of COX-1-mediated neurotoxicity in rd10 mice.

conclusionOur data suggest that the COX-1/PGE2/EP2 signaling pathway was partly responsible for significantly increased neuroinflammation and disease progression in rd10 mice, and that EP2 receptor could be targeted therapeutically to block the pathological activity of COX-1 without inducing any potential side effects in treating RP patients.

Indexed as

Disease Models, AnimalAnimalsCell LineCyclooxygenase 1Cyclooxygenase InhibitorsElectroretinographyInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPhotoreceptor CellsRetinitis PigmentosaCyclooxygenase 1Cyclooxygenase InhibitorsInflammation MediatorsCOX-1EP2 receptorNeuroinflammationPhotoreceptorsrd10 mice

Identifiers

PMID33059704
PMCPMC7565369
OpenAlexW3093393297

What OpenQuestion 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 OpenQuestion graph.