Evidence map›Paper›PMID 28290498›Full record

ArticleScientific reports2017

Inhibition of leukotriene B4 receptor 1 attenuates lipopolysaccharide-induced cardiac dysfunction: role of AMPK-regulated mitochondrial function.

Meng Sun, Rui Wang, Qinghua Han

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Adipocyte-derived LTB4 programs human NKG2AJournal for immunotherapy of cancer · 2026
    Article
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  6. Targeting AMP-activated protein kinase in sepsis.Frontiers in endocrinology · 2024
    Review
  7. Article
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  15. Resveratrol Attenuates Lipopolysaccharides (LPS)-Induced Inhibition of Osteoblast Differentiation in MC3T3-E1 Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  16. Leptin MediatesFrontiers in immunology · 2018
    Article
  17. Article
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

3 authors at 2 institutions in 1 country.

Meng SunDepartment of Cardiology, The First Hospital of Shanxi Medical University, 85 Jiefang South Road, Taiyuan 030001, China.
Rui WangDepartment of Cardiology, The First Hospital of Shanxi Medical University, 85 Jiefang South Road, Taiyuan 030001, China.
Qinghua HanDepartment of Cardiology, The First Hospital of Shanxi Medical University, 85 Jiefang South Road, Taiyuan 030001, China.
First Hospital of Shanxi Medical University · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukotriene B4 (LTB4)-mediated leukocyte recruitment and inflammatory cytokine production make crucial contributions to chronic inflammation and sepsis; however, the role of LTB4 in lipopolysaccharide (LPS)-induced cardiac dysfunction remains unclear. Therefore, the present study addressed this issue using an LTB4 receptor 1 (BLT1) inhibitor. Administration of LPS to mice resulted in decreased cardiovascular function. Inhibition of LTB4/BLT1 with the BLT1 inhibitor U75302 significantly improved survival and attenuated the LPS-induced acute cardiac dysfunction. During LPS challenge, the phosphorylated AMPK/ACC signaling pathway was slightly activated, and this effect was enhanced by U75302. Additionally, pNF-κB, Bax and cleaved caspase-3 were upregulated by LPS, and Bcl-2, IκB-α, mitochondrial complex I, complex II, and OPA1 were downregulated; however, these effects were reversed by U75302. The results indicated that the BLT1 antagonist suppressed cardiac apoptosis, inflammation, and mitochondrial impairment. Furthermore, the protection provided by the BLT1 inhibitor against LPS-induced cardiac dysfunction was significantly reversed by the AMPK inhibitor Compound C. In conclusion, inhibiting the LTB4/BLT1 signaling pathway via AMPK activation is a potential treatment strategy for septic cardiac dysfunction because it efficiently attenuates cardiac apoptosis, which may occur via the inhibition of inflammation and mitochondrial dysfunction.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein KinasesAnimalsAnti-Inflammatory Agentsbcl-2-Associated X ProteinCardiomyopathiesCardiotonic AgentsCaspase 3Fatty AlcoholsGene Expression RegulationGlycolsI-kappa B ProteinsInflammationLeukotriene B4LipopolysaccharidesMaleAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesAnti-Inflammatory AgentsBax protein, mousebcl-2-Associated X ProteinBcl2 protein, mouseCardiotonic AgentsCasp3 protein, mouseCaspase 3Fatty AlcoholsGlycolsI-kappa B ProteinsLeukotriene B4LipopolysaccharidesLtb4r1 protein, mouseNF-kappa BoxadinOxazinesProto-Oncogene Proteins c-bcl-2Receptors, Leukotriene B4U 75302

Identifiers

PMID28290498
PMCPMC5349523
OpenAlexW2713286426

What OpenQuestion holds

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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.