Evidence map›Paper›PMID 31489719›Full record

ArticleJournal of clinical laboratory analysis2020

Involvement of miR-145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells.

Wenhui Huang, Cheng Huang, Huanyu Ding, Jianfang Luo, Yuan Liu, Ruixin Fan, Fei Xiao, Xiaoping Fan, Zhisheng Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2020. 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
1.7field-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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. LINC00152/miR-145-5p/KLF4 ceRNA Axis: Diagnostic and Prognostic Value in Aortic Dissection.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Article
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  3. Article
  4. Review
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  6. Non-coding RNAs Regulate the Pathogenesis of Aortic Dissection.Frontiers in cardiovascular medicine · 2022
    Review
  7. Review
  8. 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

9 authors at 2 institutions in 1 country.

Wenhui HuangInstitute of Cardiovascular Disease and Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical School, University of South China, Hengyang, China.
Cheng HuangDepartment of Cardiology, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Huanyu DingDepartment of Cardiology, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.ORCID https://orcid.org/0000-0002-0307-9119
Jianfang LuoDepartment of Cardiology, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.ORCID https://orcid.org/0000-0003-3220-1280
Yuan LiuDepartment of Cardiology, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Ruixin FanDepartment of Cardiovascular Surgery, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Fei XiaoDepartment of Cardiovascular Surgery, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Xiaoping FanDepartment of Cardiovascular Surgery, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Zhisheng JiangInstitute of Cardiovascular Disease and Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical School, University of South China, Hengyang, China.ORCID https://orcid.org/0000-0002-0702-588X
Guangdong Academy of Medical Sciences · CNUniversity of South China · CN

Funding

High-level Hospital Construction Project DFJH201807National Natural Science Foundation of China 81300230
6 · The paper itself

Abstract

aimThe current study aimed to examine miR-145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs).

methodsThe concentration of circulating miR-145 was determined in patients with AD and healthy controls using quantitative polymerase chain reaction (qPCR). Aortic specimens were obtained from both individuals with Stanford type A AD undergoing surgical treatment and deceased organ donors (serving as controls) whose causes of death were nonvascular diseases. Then, qPCR and fluorescence in situ hybridization were applied to assess miR-145 amounts and location, respectively. Furthermore, qPCR and immunoblot were employed to determine SMAD3 (the target gene of miR-145, involved in the TGF-β pathway) amounts at the gene and protein levels, respectively. Moreover, in vitro transfection of VSMCs with miR-145 mimics or inhibitors was conducted. Finally, the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Transwell assay and flow cytometry were employed for detecting VSMC proliferation, migration, and apoptosis, respectively.

resultsThe amounts of miR-145 in plasma and aortic specimens were markedly reduced in the AD group in comparison with control values (P < .05). miR-145 was mostly located in VSMCs. Proliferation and apoptosis of VSMCs were significantly induced in vitro by the downregulation of miR-145. Also, miR-145 modulated SMAD3 expression.

conclusionsmiR-145 was found to be downregulated in patients with AD, which induced the proliferation, migration, and apoptosis of VSMCs by targeting SMAD3. This suggested the involvement of miR-145 in the pathogenesis of AD.

Indexed as

AgedAortic DissectionApoptosisBase SequenceCell MovementCell ProliferationFemaleGene Expression RegulationHumansMaleMicroRNAsMiddle AgedMuscle, Smooth, VascularMyocytes, Smooth MuscleSmad3 ProteinMicroRNAsMIRN145 microRNA, humanSmad3 ProteinSMAD3 protein, humanaortic dissectionmiR-145proliferationSMAD3vascular smooth muscle cell

Identifiers

PMID31489719
PMCPMC6977357
OpenAlexW2972157170

What OpenQuestion holds

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Registered trials

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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.