Evidence map›Paper›PMID 31391207›Full record

ArticleBioscience reports2019

C-reactive protein promotes inflammation through TLR4/NF-κB/TGF-β pathway in HL-1 cells.

Weiping Sun, Yongquan Wu, Mingyang Gao, Ying Tian, Peng Qi, Yujing Shen, Lihong Huang, Liang Shi, Yanjiang Wang, Xingpeng Liu

Expression of concernOpen access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 29 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 3 pooled it
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

29 citing papers in PubMed, 3 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  9. Article
  10. C-reactive protein-induced injury inMicrobiology spectrum · 2025
    Article
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  20. TLR4 knockdown by miRNA-140-5p improves tendinopathy: anArchives of medical science : AMS · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Weiping SunDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China.
Yongquan WuDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Mingyang GaoDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China.
Ying TianDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China.
Peng QiDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China.
Yujing ShenDepartment of Cardiology, Fuwai Hospital, Chinese academy of Medicine sciences, Beijing 100037, China.
Lihong HuangDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China.
Liang ShiDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China.
Yanjiang WangDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China.
Xingpeng LiuDepartment of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing 100037, China haebjoo1190@163.com xpliu71@vip.sina.com.ORCID 0000-0001-6493-7271
Capital Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common type of heart arrhythmia. Currently, the pathogenesis of AF is not fully understood yet. A growing body of evidence highlighted the strong association between inflammation and the pathogenesis of AF. C-reactive protein (CRP) is an inflammation marker with increased expression in AF. Therefore, the aim of this study was to determine if CRP promotes inflammation, which may sequentially mediate the onset of AF and the concurrent atrial fibrosis, through TLR4/NF-κB/TGF-β pathway. HL-1 cells were treated with either 25 or 50 μg/ml recombinant human CRP. TGF-β1 and NF-κB inhibitors were given either solely or together to the 50 μg/ml CRP-treated cells. Cell proliferation, apoptosis, the expression of apoptotic factors and TLR4, IL-6, TGF-β1, Smad2, and the phosphorylation of Smad2 were determined. Data showed that CRP induced dose-dependent inhibition on cell proliferation and promoted cell apoptosis, which was induced through both intrinsic and extrinsic pathways. Such effects were reversed by inhibiting TGF-β1 and/or NF-κB. Inhibition of TGF-β1 and/or NF-κB also reduced the expression of TLR4 and IL-6. Inhibition of NF-κB alone weakened the expression of TGF-β1 and phosphorylation of Smad2. Our study demonstrated that CRP is not only a marker, but also an important mediator in the induction of inflammation and likely the pathogenesis of AF. We for the first time reported CRP-induced activation and cross-talk between TLR4 and NF-κB/TGF-β1 signaling pathway in a cardiomyocyte model. Reducing CRP and targeting TLR4/NF-κB/TGF-β1 pathway may provide new insights in the therapeutic interventions to inflammation-induced AF.

Indexed as

Signal TransductionAtrial FibrillationCell LineC-Reactive ProteinGene Expression RegulationHumansInflammationNF-kappa BToll-Like Receptor 4Transforming Growth Factor betaC-Reactive ProteinNF-kappa BTLR4 protein, humanToll-Like Receptor 4Transforming Growth Factor betaatrial fibrillationinflammationNF-κBToll-like receptor 4transforming growth factor-beta1

Identifiers

PMID31391207
PMCPMC6712437
OpenAlexW2965483045

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.