Evidence map›Paper›PMID 33760172›Full record

ArticleMolecular medicine reports2021

Regulatory role of the TLR4/JNK signaling pathway in sepsis‑induced myocardial dysfunction.

Chao Chang, Liya Hu, Shanshan Sun, Yanqiu Song, Shan Liu, Jing Wang, Peijun Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 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
2.3field-weighted citation impact, top 12% 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, 23 citations in OpenAlex.

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  20. Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy.Frontiers in network physiology · 2022
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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

7 authors at 4 institutions in 1 country.

Chao Chang *Department of Cardiovascular Surgical ICU, Tianjin Chest Hospital, Nankai University, Tianjin 300222, P.R. China.
Liya Hu *Department of Critical Care Medicine, The Third Central Hospital of Tianjin, Tianjin 300170, P.R. China.
Shanshan SunDepartment of Emergency, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China.
Yanqiu SongTianjin Cardiovascular Institute, Tianjin Chest Hospital, Tianjin 300222, P.R. China.
Shan LiuTianjin Cardiovascular Institute, Tianjin Chest Hospital, Tianjin 300222, P.R. China.
Jing WangDepartment of Pathology, Tianjin Chest Hospital, Nankai University, Tianjin 300222, P.R. China.
Peijun LiDepartment of Cardiovascular Surgical ICU, Tianjin Chest Hospital, Nankai University, Tianjin 300222, P.R. China.
Nankai University · CNTianjin Chest Hospital · CNCangzhou Central Hospital · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a life‑threatening organ dysfunction caused by a dysregulated host response to infection, and is a leading cause of mortality worldwide. Myocardial dysfunction is associated with poor prognosis in patients with sepsis and contributes to a high risk of mortality. However, the pathophysiological mechanisms underlying sepsis‑induced myocardial dysfunction are not completely understood. The aim of the present study was to investigate the role of toll‑like receptor 4 (TLR4)/c‑Jun N‑terminal kinase (JNK) signaling in pro‑inflammatory cytokine expression and cardiac dysfunction during lipopolysaccharide (LPS)‑induced sepsis in mice. C57BL/6 mice were pretreated with TAK‑242 or saline for 1 h and then subjected to LPS (12 mg/kg, intraperitoneal) treatment. Cardiac function was assessed using an echocardiogram. The morphological changes of the myocardium were examined by hematoxylin and eosin staining and transmission electron microscopy. The serum protein levels of cardiac troponin I (cTnI) and tumor necrosis factor‑α (TNF‑α) were determined by an enzyme‑linked immunosorbent assay (ELISA). The TLR4 and JNK mRNA levels were analyzed via reverse transcription‑quantitative PCR. TLR4, JNK and phosphorylated‑JNK protein levels were measured by western blotting. In response to LPS, the activation of TLR4 and JNK in the myocardium was upregulated. There were significant increases in the serum levels of TNF‑α and cTnI, as well as histopathological changes in the myocardium and suppressed cardiac function, following LPS stimulation. Inhibition of TLR4 activation using TAK‑242 led to a decrease in the activation of JNK and reduced the protein expression of TNF‑α in plasma, and alleviated histological myocardial injury and improved cardiac function during sepsis in mice. The present data suggested that the TLR4/JNK signaling pathway played a critical role in regulating the production of pro‑inflammatory cytokines and myocardial dysfunction induced by LPS.

Indexed as

AnimalsApoptosisCytokinesDisease Models, AnimalHeart FailureHumansInterleukin-6JNK Mitogen-Activated Protein KinasesLipopolysaccharidesMAP Kinase Signaling SystemMiceMyocardiumNF-kappa BPhosphorylationSepsisToll-Like Receptor 4CytokinesInterleukin-6JNK Mitogen-Activated Protein KinasesLipopolysaccharidesNF-kappa BTlr4 protein, mouseToll-Like Receptor 4Troponin ITumor Necrosis Factor-alphaanimal modelsc‑Jun N‑terminal kinase signaling pathwaylipopolysaccharidemyocardial dysfunctionsepsisToll‑like receptor 4

Identifiers

PMID33760172
PMCPMC7974310
OpenAlexW3135610688

What OpenQuestion holds

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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.