Evidence map›Paper›PMID 30046376›Full record

ArticleOxidative medicine and cellular longevity2018

TLR4 Activation Promotes the Progression of Experimental Autoimmune Myocarditis to Dilated Cardiomyopathy by Inducing Mitochondrial Dynamic Imbalance.

Bangwei Wu, Jian Li, Huanchun Ni, Xinyu Zhuang, Zhiyong Qi, Qiying Chen, Zhichao Wen, Haiming Shi, Xinping Luo, Bo Jin

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 53 citations in OpenAlex.

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  8. OPA1, a molecular regulator of dilated cardiomyopathy.Journal of cellular and molecular medicine · 2023
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  15. Exosome-mediated lnc-ABCA12-3 promotes proliferation and glycolysis but inhibits apoptosis by regulating the toll-like receptor 4/nuclear factor kappa-B signaling pathway in esophageal squamous cell carcinoma.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
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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.

Bangwei WuDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0002-2765-4640
Jian LiDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Huanchun NiDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Xinyu ZhuangDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Zhiyong QiDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China.
Qiying ChenDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Zhichao WenDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0002-5399-8957
Haiming ShiDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Xinping LuoDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0001-9484-9467
Bo JinDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0002-2911-7144
Fudan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dynamic imbalance associates with several cardiovascular diseases. However, the role of mitochondrial dynamics in TLR4 activation-mediated dilated cardiomyopathy (DCM) progress remains unknown. A model of experimental autoimmune myocarditis (EAM) was established in BALB/c mice on which TLR4 activation by LPS-EB or TLR4 inhibition by LPS-RS was performed to induce chronic inflammation for 5 weeks. TLR4 activation promoted the transition of EAM to DCM as demonstrated by increased cardiomyocyte apoptosis, myocardial fibrosis, ventricular dilatation, and declined heart function. TLR4 inhibition mitigated the above DCM changes. Transmission electron microscope study showed that mitochondria became fragmented, also with damaged crista in ultrastructure in EAM mice. TLR4 activation aggravated the above mitochondrial aberration, and TLR4 inhibition alleviated it. The mitochondrial dynamic imbalance and damage in DCM development were mainly associated with OPA1 downregulation, which may be caused by elevated TNF-

Indexed as

Adenosine TriphosphateAnimalsApoptosisAutoimmune DiseasesBlotting, WesternCardiomyopathy, DilatedEchocardiographyEnzyme-Linked Immunosorbent AssayFlow CytometryImmunohistochemistryLipid PeroxidationMaleMetalloproteasesMiceMice, Inbred BALB CMicroscopy, Electron, TransmissionAdenosine TriphosphateMetalloproteasesMitochondrial ProteinsOMA1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID30046376
PMCPMC6038665
OpenAlexW2811394603

What OpenQuestion holds

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LicenceCC BY
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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.