Evidence map›Paper›PMID 37232575›Full record

ArticleActa biochimica et biophysica Sinica2023

Bioinformatics exploration of potential common therapeutic targets for systemic and pulmonary arterial hypertension-induced myocardial hypertrophy.

Lu Chen, Mingjue Li, Mengjia Shen, Yingqi Zhu, Kaitong Chen, Xiaoxia Huang, Cankun Zheng, Qiancheng Wang, Hairuo Lin, Wangjun Liao and 3 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
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

13 authors at 2 institutions in 1 country.

Lu ChenDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Mingjue LiDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Mengjia ShenDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yingqi ZhuDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Kaitong ChenDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Xiaoxia HuangDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Cankun ZhengDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Qiancheng WangDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Hairuo LinDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Wangjun LiaoDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Jianping BinDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Siyuan MaDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yulin LiaoDepartment of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Province Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Southern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic and pulmonary arterial hypertension (PAH) can induce left and right ventricular hypertrophy, respectively, but common therapeutic targets for both left and right hypertrophy are limited. In this study, we attempt to explore potential common therapeutic targets and screen out potential target drugs for further study. Cardiac mRNA expression profiles in mice with transverse aortic constriction (TAC) and pulmonary arterial constriction (PAC) are obtained from online databases. After bioinformatics analyses, we generate TAC and PAC mouse models to validate the phenotypes of cardiac remodelling as well as the identified hub genes. Bioinformatics analyses show that there are 214 independent differentially expressed genes (DEGs) in GSE136308 (TAC related) and 2607 independent DEGs in GSE30922 (PAC related), while 547 shared DEGs are associated with the function of the extracellular matrix (ECM) or involved in the PI3K-Akt signaling pathway, cytokine-cytokine receptor interactions, and ECM-receptor interactions. We identifyd

Indexed as

Hypertrophy, Left VentricularPulmonary Arterial HypertensionAnimalsCardiomegalyCollagen Type IComputational BiologyDehydroepiandrosteroneFibrosisHypertrophy, Right VentricularMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesVentricular RemodelingCollagen Type ICollagen Type I, alpha2 SubunitDehydroepiandrosteronePhosphatidylinositol 3-Kinasesbioinformaticshub genemyocardial fibrosismyocardial hypertrophypressure overload

Identifiers

PMID37232575
PMCPMC10281875
OpenAlexW4365455790

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.