Evidence map›Paper›PMID 30233845›Full record

ArticleJournal of thoracic disease2018

Deletion of ACTA2 in mice promotes angiotensin II induced pathogenesis of thoracic aortic aneurysms and dissections.

Jiancheng Cheng, Xianwu Zhou, Xionggang Jiang, Tucheng Sun

Open access · hybridAbstract read
In one paragraph

Article in Journal of thoracic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 27 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

4 authors at 4 institutions in 1 country.

Jiancheng ChengDepartment of Cardiothoracic Surgery, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China.
Xianwu ZhouDepartment of Cardiovascular Surgery, Wuhan Asia Heart Hospital, Wuhan 430015, China.
Xionggang JiangDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Tucheng SunGuangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China.
Guangdong General Hospital · CNUnion Hospital · CNWuhan Asia Heart Hospital · CNZhengzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMutation of the ACTA2 (α-2 smooth muscle actin) gene accounts for ~15% of all cases of familial thoracic aortic aneurysms and dissections. Surprisingly, no severe vascular phenotypes were observed at baseline in mice carrying this gene mutation. Our aim was to explore whether mutation of ACTA2 promotes the development of aneurysms or dissections in the presence of angiotensin II (AngII) and to determine whether this mutation has an impact on the phenotypic modulation and apoptosis mediated by AngII in vascular smooth muscle cells (VSMCs).

methodsMice were divided into three groups: AngII stimulated-wild-type (WT) (AngII) and ACTA2

resultsCompared with the AngII- group, the ACTA2 mice exhibited more severity of dilated lumena of the aortas, a significantly increased expression of osteopontin (OPN), an elevated ratio of Bax/Bcl-2, increased apoptosis, and a decreased expression of α-smooth muscle actin (α-SMA).

conclusionsKnockout of ACTA2 promoted AngII induced progressive lumen dilation of the aortas, apoptosis, and the phenotypic modulation in VSMCs in mice.

Indexed as

Aortic aneurysmaortic dissectiongene mutationsmooth muscle actin alpha 2 (ACTA2)

Identifiers

PMID30233845
PMCPMC6129878
OpenAlexW2888013149

What OpenQuestion holds

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Read underepoch 390

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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.