Evidence map›Paper›PMID 32699607›Full record

ArticlePulmonary circulation

hsa-miR-106b-5p participates in the development of chronic thromboembolic pulmonary hypertension via targeting matrix metalloproteinase 2.

Ran Miao, Xingbei Dong, Juanni Gong, Ying Wang, Xiaojuan Guo, Yidan Li, Min Liu, Jun Wan, Jifeng Li, Suqiao Yang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Pulmonary circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 17 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

15 authors at 3 institutions in 2 countries.

Ran MiaoMedical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Xingbei DongWest China School of Medicine/West China Hospital, Sichuan University, Chengdu, China.
Juanni GongKey Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing, China.
Ying WangDepartment of Pathology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Xiaojuan GuoDepartment of Radiology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Yidan LiDepartment of Echocardiography, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Min LiuDepartment of Radiology, China-Japan Friendship Hospital, Beijing, China.ORCID https://orcid.org/0000-0003-1298-4441
Jun WanKey Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing, China.
Jifeng LiKey Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing, China.
Suqiao YangKey Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing, China.ORCID https://orcid.org/0000-0001-7369-5999
Wang WangDepartment of Physiology and Pathophysiology, Capital Medical University, Beijing, China.
Tuguang KuangKey Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing, China.
Jiuchang ZhongHeart Center and Beijing Key Laboratory of Hypertension, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Zhenguo ZhaiKey Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing, China.
Yuanhua YangKey Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing, China.ORCID https://orcid.org/0000-0002-4197-9097
Capital Medical University · CNChina-Japan Friendship Hospital · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic thromboembolic pulmonary hypertension (CTEPH) is characterized by elevated pressure in pulmonary arteries. This study was performed to explore the critical miRNAs and genes affecting the pathogenesis of CTEPH.

methodsGSE56914 dataset (10 CTEPH whole blood samples and 10 control samples) was downloaded from the Gene Expression Omnibus database. Using limma package, the differentially expressed miRNAs (DE-miRNAs) were acquired. After miRNA-target pairs were obtained using miRWalk2.0 tool, a miRNA-target regulatory network was built by Cytoscape software. Using DAVID tool, significantly enriched pathways involving the target genes were identified. Moreover, the protein-protein interaction network and transcription factor-target regulatory network were built by the Cytoscape software. Additionally, quantitative real-time PCR (qRT-PCR) experiments and luciferase assay were conducted to validate miRNA/gene expression and miRNA-target regulatory relationship, respectively.

resultsThere were 25 DE-miRNAs (8 up-regulated and 17 down-regulated) between CTEPH and control groups. The target genes of has-let-7b-3p, has-miR-17-5p, has-miR-3202, has-miR-106b-5p, and has-miR-665 were enriched in multiple pathways such as "Insulin secretion". qRT-PCR analysis confirmed upregulation of hsa-miR-3202, hsa-miR-665, and matrix metalloproteinase 2 (

conclusionsThese miRNAs and genes were associated with the pathogenesis of CTEPH. Besides, hsa-miR-106b-5p was involved in the development of CTEPH via targeting

Indexed as

chronic thromboembolic pulmonary hypertensiondifferentially expressed miRNAsluciferase assayprotein–protein interaction networkregulatory networktarget genes

Identifiers

PMID32699607
PMCPMC7357097
OpenAlexW3041615342

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.