Evidence map›Paper›PMID 31880857›Full record

ArticleJournal of cellular and molecular medicine2020

Up-regulation of paired-related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a.

Wen-Wu Bai, Zhen-Yu Tang, Ti-Chao Shan, Xue-Jiao Jing, Peng Li, Wei-Dong Qin, Ping Song, Bo Wang, Jian Xu, Zhan Liu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-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

21 citing papers in PubMed, 36 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 7 institutions in 1 country.

Wen-Wu BaiThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, China.
Zhen-Yu TangDepartment of Emergency, Qilu Hospital of Shandong University, Jinan, China.
Ti-Chao ShanDepartment of Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, China.
Xue-Jiao JingDepartment of Geriatric Medicine, Qilu Hospital of Shandong University, Key Laboratory of Cardiovascular Proteomics of Shandong Province, Qilu Hospital of Shandong University, Jinan, China.
Peng LiDepartment of Pharmacology, College of Pharmacy, Xinxiang Medical University, Xinxiang, China.
Wei-Dong QinDepartment of Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, China.ORCID 0000-0001-7238-6860
Ping SongDepartment of Pharmacology, College of Pharmacy, Xinxiang Medical University, Xinxiang, China.
Bo WangDepartment of Traditional Chinese Medicine, Qilu Hospital of Shandong University, Jinan, China.
Jian XuDepartment of Pharmacology, College of Pharmacy, Xinxiang Medical University, Xinxiang, China.
Zhan LiuDepartment of Gastroenterology and Clinical Nutrition, The First Affiliated Hospital of Hunan Normal University, Changsha, China.ORCID 0000-0001-5214-1284
Hai-Ya YuDepartment of Neurology, The People's Hospital of Xishui County, Huangang, China.
Zhi-Min MaDepartment of Endocrinology, The Affiliated Suzhou Science & Technology Town Hospital of Nanjing Medical University, Suzhou, China.
Shuang-Xi WangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, China.ORCID 0000-0003-3275-7916
Chao LiuDepartment of Neurology, The People's Hospital of Xishui County, Huangang, China.
Tao GuoThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, China.ORCID 0000-0002-5545-4240
Qilu Hospital of Shandong University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNXinxiang Medical University · CNHubei University of Science and Technology · CNHunan Normal University · CNNanjing Medical University · CNXiangshan County First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibrosis is a key factor to determine the prognosis in patient with myocardial infarction (MI). The aim of this study is to investigate whether the transcriptional factor paired-related homeobox 2 (Prrx2) regulates Wnt5a gene expression and the role in myocardial fibrosis following MI. The MI surgery was performed by ligation of left anterior descending coronary artery. Cardiac remodelling was assessed by measuring interstitial fibrosis performed with Masson staining. Cell differentiation was examined by analysis the expression of alpha-smooth muscle actin (α-SMA). Both Prrx2 and Wnt5a gene expressions were up-regulated in mice following MI, accompanied with increased mRNA and protein levels of α-SMA, collagen I and collagen III, compared to mice with sham surgery. Adenovirus-mediated gene knock down of Prrx2 increased survival rate, alleviated cardiac fibrosis, decreased infarction sizes and improved cardiac functions in mice with MI. Importantly, inhibition of Prrx2 suppressed ischaemia-induced Wnt5a gene expression and Wnt5a signalling. In cultured cardiac fibroblasts, TGF-β increased gene expressions of Prrx2 and Wnt5a, and induced cell differentiations, which were abolished by gene silence of either Prrx2 or Wnt5a. Further, overexpression of Prrx2 or Wnt5a mirrored the effects of TGF-β on cell differentiations of cardiac fibroblasts. Gene silence of Wnt5a also ablated cell differentiations induced by Prrx2 overexpression in cardiac fibroblasts. Mechanically, Prrx2 was able to bind with Wnt5a gene promoter to up-regulate Wnt5a gene expression. In conclusions, targeting Prrx2-Wnt5a signalling should be considered to improve cardiac remodelling in patients with ischaemic heart diseases.

Indexed as

AnimalsCell DifferentiationCollagen Type ICollagen Type IIIFibroblastsFibrosisGene Expression RegulationHeartHomeodomain ProteinsMaleMiceMyocardial InfarctionMyocardiumMyofibroblastsPromoter Regions, GeneticSignal TransductionCollagen Type ICollagen Type IIIHomeodomain ProteinsPrrx2 protein, mouseTransforming Growth Factor beta1Wnt-5a ProteinWnt5a protein, mousecardiac fibrosiscell differentiationmyocardial infarctionpaired-related homeobox 2Wnt5a

Identifiers

PMID31880857
PMCPMC7011146
OpenAlexW2997650794

What OpenQuestion 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 OpenQuestion graph.