Evidence map›Paper›PMID 29290979›Full record

ArticleOncotarget2017

Exacerbation of diabetic cardiac hypertrophy in OVE26 mice by angiotensin II is associated with JNK/c-Jun/miR-221-mediated autophagy inhibition.

Ling-Bo Qian, Sai-Zhi Jiang, Xiao-Qiang Tang, Jian Zhang, Ya-Qin Liang, Hai-Tao Yu, Jing Chen, Zheng Xu, Rui-Ming Liu, Bradley B Keller and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

11 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

12 authors at 7 institutions in 2 countries.

Ling-Bo QianCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
Sai-Zhi JiangPediatric Research Institute, Department of Pediatrics of the University of Louisville, Louisville, Kentucky 40202, USA.
Xiao-Qiang TangCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
Jian ZhangCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
Ya-Qin LiangPediatric Research Institute, Department of Pediatrics of the University of Louisville, Louisville, Kentucky 40202, USA.
Hai-Tao YuCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
Jing ChenPediatric Research Institute, Department of Pediatrics of the University of Louisville, Louisville, Kentucky 40202, USA.
Zheng XuCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
Rui-Ming LiuPulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama 35294, USA.
Bradley B KellerCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
Hong-Lei JiCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
Lu CaiCardiovascular Center, The First Hospital of Jilin University, Changchun 130021, China.
University of Louisville · USJilin University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNHangzhou Medical College · CNKosair Charities · USUniversity of Alabama at Birmingham · USWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both diabetes and angiotensin II (Ang II) excess trigger cardiac remodeling and dysfunction, and diabetic cardiomyopathy. We hypothesized that cardiac hypertrophy associated with the development of diabetic cardiomyopathy is worsened by increased Ang II. Male type 1 diabetic OVE26 and wild-type mice were given Ang II (sc., 1.15 mg/kg, twice a day) for 14 days. Diabetes-induced cardiac dysfunction and hypertrophy was exacerbated by Ang II treatment as determined by echocardiography, wheat germ agglutinin staining and atrial natriuretic peptide. Ang II treatment dramatically exacerbated diabetes-caused decreased LC3-II, a marker of autophagy, and increased p62, an indicator of cytosolic protein clearance. Ang II treatment also augmented diabetes-associated increased phosphorylated levels of c-Jun, JNK, mTOR, and miR-221, and decreased of p27 expression, a direct target of miR-221. Chromatin immunoprecipitation assay showed that Ang II elevated c-Jun binding to the promoter of

Indexed as

angiotensin IIautophagydiabeteshypertrophyMiR-221

Identifiers

PMID29290979
PMCPMC5739764
OpenAlexW2759247560

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.