Evidence map›Paper›PMID 25048039›Full record

ArticlePloS one2014

AMPK-NF-κB axis in the photoreceptor disorder during retinal inflammation.

Mamoru Kamoshita, Yoko Ozawa, Shunsuke Kubota, Seiji Miyake, Chiduru Tsuda, Norihiro Nagai, Kenya Yuki, Shigeto Shimmura, Kazuo Umezawa, Kazuo Tsubota

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  7. Review
  8. Article
  9. Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Targeting Neurovascular Interaction in Retinal Disorders.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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

10 authors at 2 institutions in 1 country.

Mamoru KamoshitaLaboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; Department of Ophthalmology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Yoko OzawaLaboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; Department of Ophthalmology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Shunsuke KubotaLaboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; Department of Ophthalmology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Seiji MiyakeLaboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Chiduru TsudaLaboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Norihiro NagaiLaboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; Department of Ophthalmology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Kenya YukiLaboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; Department of Ophthalmology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Shigeto ShimmuraDepartment of Ophthalmology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Kazuo UmezawaDepartment of Molecular Target Medicine Screening, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
Kazuo TsubotaDepartment of Ophthalmology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
Keio University · JPAichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent progress in molecular analysis has revealed the possible involvement of multiple inflammatory signaling pathways in pathogenesis of retinal degeneration. However, how aberrant signaling pathways cause tissue damage and dysfunction is still being elucidated. Here, we focus on 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK), originally recognized as a key regulator of energy homeostasis. AMPK is also modulated in response to inflammatory signals, although its functions in inflamed tissue are obscure. We investigated the role of activated AMPK in the retinal neural damage and visual function impairment caused by inflammation. For this purpose, we used a mouse model of lipopolysaccharide-induced inflammation in the retina, and examined the effects of an AMPK activator, 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR). During inflammation, activated AMPK in the neural retina was decreased, but AICAR treatment prevented this change. Moreover, the electroretinogram (ERG) a-wave response, representing photoreceptor function, showed visual dysfunction in this model that was prevented by AICAR. Consistently, the model showed shortened photoreceptor outer segments (OSs) with reduced levels of rhodopsin, a visual pigment concentrated in the OSs, in a post-transcriptional manner, and these effects were also prevented by AICAR. In parallel, the level of activated NF-κB increased in the retina during inflammation, and this increase was suppressed by AICAR. Treatment with an NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ) preserved the rhodopsin level during inflammation, suppressing NF-κB. These findings indicated that AMPK activation by AICAR and subsequent NF-κB inhibition had a protective effect on visual function, and that AMPK activation played a neuroprotective role during retinal inflammation.

Indexed as

Adenylate KinaseAminoimidazole CarboxamideAnimalsElectroretinographyInflammationMaleMiceNF-kappa BPhotoreceptor CellsRetinal DiseasesRhodopsinRibonucleotidesSignal TransductionAdenylate KinaseAICA ribonucleotideAminoimidazole CarboxamideNF-kappa BRhodopsinRibonucleotides

Identifiers

PMID25048039
PMCPMC4105543
OpenAlexW2000037414

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.