Evidence map›Paper›PMID 34016786›Full record

ArticleAging2021

Integrated bioinformatic analysis reveals the underlying molecular mechanism of and potential drugs for pulmonary arterial hypertension.

Haoru Dong, Xiuchun Li, Mengsi Cai, Chi Zhang, Weiqi Mao, Ying Wang, Qian Xu, Mayun Chen, Liangxing Wang, Xiaoying Huang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 33 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

10 authors at 2 institutions in 1 country.

Haoru DongThe First Clinical Medical College, Wenzhou Medical University, Wenzhou 325000, Zhejiang, P.R. China.
Xiuchun LiDivision of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University, Key Laboratory of Heart and Lung, Wenzhou 325000, Zhejiang, P.R. China.
Mengsi CaiDivision of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University, Key Laboratory of Heart and Lung, Wenzhou 325000, Zhejiang, P.R. China.
Chi ZhangThe First Clinical Medical College, Wenzhou Medical University, Wenzhou 325000, Zhejiang, P.R. China.
Weiqi MaoThe First Clinical Medical College, Wenzhou Medical University, Wenzhou 325000, Zhejiang, P.R. China.
Ying WangThe First Clinical Medical College, Wenzhou Medical University, Wenzhou 325000, Zhejiang, P.R. China.
Qian XuThe First Clinical Medical College, Wenzhou Medical University, Wenzhou 325000, Zhejiang, P.R. China.
Mayun ChenDivision of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University, Key Laboratory of Heart and Lung, Wenzhou 325000, Zhejiang, P.R. China.
Liangxing WangDivision of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University, Key Laboratory of Heart and Lung, Wenzhou 325000, Zhejiang, P.R. China.
Xiaoying HuangDivision of Pulmonary Medicine, The First Affiliated Hospital of Wenzhou Medical University, Key Laboratory of Heart and Lung, Wenzhou 325000, Zhejiang, P.R. China.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a devastating cardiovascular disease without a clear mechanism or drugs for treatment. Therefore, it is crucial to reveal the underlying molecular mechanism and identify potential drugs for PAH. In this study, we first integrated three human lung tissue datasets (GSE113439, GSE53408, GSE117261) from GEO. A total of 151 differentially expressed genes (DEGs) were screened, followed by KEGG and GO enrichment analyses and PPI network construction. Five hub genes (CSF3R, NT5E, ANGPT2, FGF7, and CXCL9) were identified by Cytoscape (Cytohubba). GSEA and GSVA were performed for each hub gene to uncover the potential mechanism. Moreover, to repurpose known and therapeutic drugs, the CMap database was retrieved, and nine candidate compounds (lypressin, ruxolitinib, triclabendazole, L-BSO, tiaprofenic acid, AT-9283, QL-X-138, huperzine-a, and L-741742) with a high level of confidence were obtained. Then ruxolitinib was selected to perform molecular docking simulations with ANGPT2, FGF7, NT5E, CSF3R, JAK1, JAK2, JAK3, TYK2. A certain concentration of ruxolitinib could inhibit the proliferation and migration of rat pulmonary artery smooth muscle cells (rPASMCs)

Indexed as

Computational BiologyAnimalsCell HypoxiaCell MovementCell ProliferationGene Expression ProfilingGene OntologyGene Regulatory NetworksHumansMolecular Docking SimulationMyocytes, Smooth MuscleNitrilesPrincipal Component AnalysisProtein Interaction MapsPulmonary Arterial HypertensionPulmonary ArteryNitrilesPyrazolesPyrimidinesruxolitinibbioinformaticsDEGshub genemolecular dockingPAHpotential drugs

Identifiers

PMID34016786
PMCPMC8202883
OpenAlexW3160010868

What Socratic holds

Textmetadata
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 Socratic graph.