Evidence map›Paper›PMID 33547400›Full record

ArticleScientific reports2021

(Pro)renin receptor involves in myocardial fibrosis and oxidative stress in diabetic cardiomyopathy via the PRR-YAP pathway.

Shiran Yu, Xuefei Dong, Min Yang, Qingtao Yu, Jie Xiong, Jing Chen, Bo Dong, Qing Su

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 20 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

8 authors at 4 institutions in 2 countries.

Shiran Yu *Department of Cardiology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Xuefei Dong *Department of Cardiology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Min Yang *Department of Cardiology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Qingtao YuDepartment of Cardiology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Jie XiongDepartment of Cardiology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Jing ChenWarwick Medical School, University of Warwick, Coventry, UK.
Bo DongDepartment of Cardiology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China. bodong@sdu.edu.cn.
Qing SuDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200092, China. suqing@xinhuamed.com.cn.
Shandong Provincial Hospital · CNShandong University · CNUniversity of Warwick · GBXinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

(Pro)renin receptor (PRR) and Yes-associated protein (YAP) play an important role in cardiovascular diseases. However, the role of PRR-YAP pathway in the pathogenesis of DCM is also not clear. We hypothesized that PRR-YAP pathway may promote pathological injuries in DCM by triggering redox. Wistar rats and neonatal rat cardiac fibroblasts were respectively used in vivo and in vitro studies. In order to observe the effects of PRR mediated YAP pathway on the pathogenesis of DCM, animal experiments were divided into 3 parts, including the evaluation the effects of PRR overexpression, PRR RNAi silencing and YAP RNAi silencing. Recombinant-adenoviruses-carried-PRR-gene (Ad-PRR), Ad-PRR-shRNA and lentivirus-carried-YAP-shRNA were constructed and the effects of PRR mediated YAP on the pathogenesis of DCM were evaluated. YAP specific inhibitor Verteporfin was also administrated in cardiac fibroblasts to explore the impact of PRR-YAP pathway on oxidative stress and myocardial fibrosis. The results displayed that PRR overexpression could enhance YAP expression but PRR RNAi silencing down-regulated its expression. Moreover, PRR overexpression could exacerbate oxidative stress and myocardial fibrosis in DCM, and these pathological changes could be rescued by YAP blockade. We concluded that PRR-YAP pathway plays a key role in the pathogenesis of DCM.

Indexed as

Oxidative StressAnimalsDiabetic CardiomyopathiesFibrosisIntracellular Signaling Peptides and ProteinsMaleMyocardiumProrenin ReceptorRatsRats, WistarReceptors, Cell SurfaceSignal TransductionVacuolar Proton-Translocating ATPasesYAP-Signaling ProteinsATP6AP2 protein, ratIntracellular Signaling Peptides and ProteinsProrenin ReceptorReceptors, Cell SurfaceVacuolar Proton-Translocating ATPasesYap1 protein, ratYAP-Signaling Proteins

Identifiers

PMID33547400
PMCPMC7865047
OpenAlexW3127779323

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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.