Evidence map›Paper›PMID 28469203›Full record

ArticleScientific reports2017

Involvement of the MEK-ERK/p38-CREB/c-fos signaling pathway in Kir channel inhibition-induced rat retinal Müller cell gliosis.

Feng Gao, Fang Li, Yanying Miao, Lin-Jie Xu, Yuan Zhao, Qian Li, Sheng-Hai Zhang, Jihong Wu, Xing-Huai Sun, Zhongfeng Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

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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 3 institutions in 1 country.

Feng GaoDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Fang LiInstitutes of Brain Science and State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, 200032, China.
Yanying MiaoInstitutes of Brain Science and State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, 200032, China.
Lin-Jie XuDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Yuan ZhaoDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Qian LiDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Sheng-Hai ZhangDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Jihong WuDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Xing-Huai SunDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China. xhsun@shmu.edu.cn.
Zhongfeng WangDepartment of Ophthalmology at Eye & ENT Hospital, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China. zfwang@fudan.edu.cn.
Eye & ENT Hospital of Fudan University · CNFudan University · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous studies have demonstrated that activation of group I metabotropic glutamate receptors downregulated Kir channels in chronic ocular hypertension (COH) rats, thus contributing to Müller cell gliosis, characterized by upregulated expression of glial fibrillary acidic protein (GFAP). In the present study, we explored possible signaling pathways linking Kir channel inhibition and GFAP upregulation. In normal retinas, intravitreal injection of BaCl

Indexed as

Signal TransductionAnimalsBarium CompoundsButadienesChloridesChronic DiseaseCyclic AMP Response Element-Binding ProteinDisease Models, AnimalEpendymoglial CellsGene Expression RegulationGlial Fibrillary Acidic ProteinGliosisJNK Mitogen-Activated Protein KinasesMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3barium chlorideBarium CompoundsButadienesChloridesCyclic AMP Response Element-Binding ProteinGfap protein, ratGlial Fibrillary Acidic ProteinJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Nitrilesp38 Mitogen-Activated Protein KinasesPotassium Channels, Inwardly RectifyingProtein Kinase InhibitorsProto-Oncogene Proteins c-fosU 0126

Identifiers

PMID28469203
PMCPMC5431154
OpenAlexW2608607590

What OpenQuestion holds

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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.