Evidence map›Paper›PMID 32119711›Full record

ArticlePloS one2020

Angiotensin II promotes podocyte injury by activating Arf6-Erk1/2-Nox4 signaling pathway.

Guanghua Che, Hang Gao, Qibo Hu, Hongchang Xie, Yunfeng Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.2field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  11. The Perspective of Vitamin D on suPAR-Related AKI in COVID-19.International journal of molecular sciences · 2022
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  14. Mechanism of Albuminuria Reduction by Chymase Inhibition in Diabetic Mice.International journal of molecular sciences · 2020
    Article
  15. 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

5 authors at 2 institutions in 1 country.

Guanghua CheDepartment of Pediatrics, Second Hospital, Jilin University, Changchun, China.
Hang GaoThe Key Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Qibo HuDepartment of Pediatrics, Second Hospital, Jilin University, Changchun, China.
Hongchang XieDepartment of Pediatrics, Second Hospital, Jilin University, Changchun, China.
Yunfeng ZhangDepartment of Pediatrics, Second Hospital, Jilin University, Changchun, China.ORCID 0000-0001-7941-1280
Second Affiliated Hospital of Jilin University · CNFirst Bethune Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin II (Ang II) is a key contributor to glomerular disease by predominantly resulting in podocyte injury, whereas the underlying molecular mechanisms has not been fully understood. This study aimed to investigate if and how ADP-ribosylation factor 6 (Arf6), a small GTP-binding protein, involves Ang II-induced cellular injury in cultured human podocytes. Cellular injury was evaluated with caspase 3 activity, reactive oxygen species (ROS) level and TUNEL assay. Arf6 activity was measured using an Arf6-GTP Pull-Down Assay. Ang II significantly enhanced Arf6 expressions accompanied by increase of Arf6-GTP. The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor. Induction of ROS by Ang II was inhibited in podocytes with Nox4 knockdown. Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown. Phpspho-Erk1/2Thr202/Tyr204 levels were upregulated remarkably following Ang II treatment, and Erk inhibitor LY3214996 significantly downregulated Nox4 expression. In addition, Ang II decreased CD2AP expression. Overexpression of CD2AP prevented Ang II-induced upregulation of Arf6-GTP. Our data demonstrated that Ang II promotes ROS production and podocytes injury through activation of Arf6-Erk1/2-Nox4 signaling. We also provided evidence that Ang II activates Arf6 by degradation of CD2AP.

Indexed as

MAP Kinase Signaling SystemAdaptor Proteins, Signal TransducingADP-Ribosylation Factor 6ADP-Ribosylation FactorsAngiotensin IICytoskeletal ProteinsDown-RegulationGuanosine TriphosphateHumansNADPH Oxidase 4PodocytesReactive Oxygen SpeciesAdaptor Proteins, Signal TransducingADP-Ribosylation Factor 6ADP-Ribosylation FactorsAngiotensin IIARF6 protein, humanCD2-associated proteinCytoskeletal ProteinsGuanosine TriphosphateNADPH Oxidase 4Reactive Oxygen Species

Identifiers

PMID32119711
PMCPMC7051060
OpenAlexW3009809333

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.