Evidence map›Paper›PMID 26415877›Full record

ArticleScientific reports2015

Downregulating p22phox ameliorates inflammatory response in Angiotensin II-induced oxidative stress by regulating MAPK and NF-κB pathways in ARPE-19 cells.

Yiguo Qiu, Lifei Tao, Chunyan Lei, Jiaming Wang, Peizeng Yang, Qiuhong Li, Bo Lei

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  7. Regulation of Superoxide by BAP31 through Its Effect on p22Oxidative medicine and cellular longevity · 2021
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  18. Activation of liver X receptor α protects amyloid βInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
  19. 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

7 authors at 3 institutions in 2 countries.

Yiguo QiuDepartment of Ophthalmology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, China.
Lifei TaoDepartment of Ophthalmology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, China.
Chunyan LeiDepartment of Ophthalmology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, China.
Jiaming WangDepartment of Ophthalmology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, China.
Peizeng YangDepartment of Ophthalmology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, China.
Qiuhong LiDepartment of Ophthalmology, University of Florida, Gainesville, Florida, USA.
Bo LeiDepartment of Ophthalmology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and inflammation are two interrelated biological events implicated in the pathogenesis of many diseases. Reactive oxygen species (ROS) produced under oxidative stress play a key role in pathological conditions. Inhibition of p22phox, an indispensable component of the NADPH oxidase (NOX) complex comprising the main source of ROS, plays a protective role in many ocular conditions by inhibiting the activation of NOXs and the generation of ROS. However, little is understood regarding the role of p22phox in oxidative stress-related inflammation in the eye. We used a p22phox small interfering RNA (siRNA) to transfect the retinal pigment epithelium (RPE)-derived cell line ARPE-19, and human primary RPE (hRPE) cells, then stimulated with Ang II. We observed a potent anti-inflammatory effect and studied the underlying mechanism. Downregulating p22phox resulted in decreased ROS generation, a reduction of NOXs (NOX1, 2, 4) and a decrease in inflammatory cytokine. In addition, p22phox downregulation reduced the activation of the MAPK and NF-κB signaling pathways. We conclude that inhibition of p22phox has an anti-inflammatory effect in Ang II-induced oxidative stress. Suppressing the MAPK and NF-κB pathways is involved in this protective effect. These results suggest that p22phox may provide a promising therapeutic target for oxidative stress-induced ocular inflammation.

Indexed as

Angiotensin IICell LineChemokine CCL2Epithelial CellsGene Expression RegulationHumansInflammationInterleukin-6Interleukin-6 InhibitorsInterleukin-8Membrane GlycoproteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADPH Oxidase 1NADPH Oxidase 2NADPH Oxidase 4Angiotensin IICCL2 protein, humanChemokine CCL2CYBA protein, humanCYBB protein, humanIL6 protein, humanInterleukin-6Interleukin-6 InhibitorsInterleukin-8MAPK1 protein, humanMembrane GlycoproteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADPH Oxidase 1NADPH Oxidase 2NADPH Oxidase 4NADPH OxidasesNF-kappa BNOX1 protein, humanNOX4 protein, humanp38 Mitogen-Activated Protein KinasesRNA, Small Interfering

Identifiers

PMID26415877
PMCPMC4586461
OpenAlexW2253391583

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.