Evidence map›Paper›PMID 25396421›Full record

ArticlePloS one2014

Protective role of the cholinergic anti-inflammatory pathway in a mouse model of viral myocarditis.

Zheng Cheng, Ge Li-Sha, Zhao Jing-Lin, Zhang Wen-Wu, Chen Xue-Si, Chen Xing-Xing, Li Yue-Chun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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, 36 citations in OpenAlex.

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  11. Electroacupuncture Improves the Survival Rate and Organ Function in a Rat Model of Hemorrhagic Shock.Evidence-based complementary and alternative medicine : eCAM · 2019
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  15. Frontiers in pediatrics · 2018
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  16. Article
  17. Calumenin relieves cardiac injury by inhibiting ERS-initiated apoptosis during viral myocarditis.International journal of clinical and experimental pathology · 2017
    Review
  18. Article
  19. Article
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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 1 institution in 1 country.

Zheng ChengDepartment of Cardiology, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Ge Li-ShaDepartment of Pediatric, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Zhao Jing-LinDepartment of Cardiology, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Zhang Wen-WuDepartment of Cardiology, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Chen Xue-SiDepartment of Cardiology, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Chen Xing-XingDepartment of Cardiology, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Li Yue-ChunDepartment of Cardiology, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivation of the cholinergic anti-inflammatory pathway, which relies on the α7nAchR (alpha 7 nicotinic acetylcholine receptor), has been shown to decrease proinflammatory cytokines. This relieves inflammatory responses and improves the prognosis of patients with experimental sepsis, endotoxemia, ischemia/reperfusion injury, hemorrhagic shock, pancreatitis, arthritis and other inflammatory syndromes. However, whether the cholinergic anti-inflammatory pathway has an effect on acute viral myocarditis has not been investigated. Here, we studied the effects of the cholinergic anti-inflammatory pathway on acute viral myocarditis. METHODOLOGY/PRINCIPAL

findingsIn a coxsackievirus B3 murine myocarditis model (Balb/c), nicotine and methyllycaconitine were used to stimulate and block the cholinergic anti-inflammatory pathway, respectively. Relevant signal pathways were studied to compare their effects on myocarditis, survival rate, histopathological changes, ultrastructural changes, and cytokine levels. Nicotine treatments significantly improved survival rate, attenuated myocardial lesions, and downregulated the expression of TNF-α and IL-6. Methyllycaconitine decreased survival rate, aggravated myocardial lesions, and upregulated the expression of TNF-α and IL-6. In addition, levels of the signaling protein phosphorylated STAT3 were higher in the nicotine group and lower in the methyllycaconitine group compared with the untreated myocarditis group. CONCLUSIONS/SIGNIFICANCE: These results show that nicotine protects mice from CVB3-induced viral myocarditis and that methyllycaconitine aggravates viral myocarditis in mice. Because nicotine is a α7nAchR agonist and methyllycaconitine is a α7nAchR antagonist, we conclude that α7nAchR activation increases the phosphorylation of STAT3, reduces the expression of TNF-α and IL-6, and, ultimately, alleviates viral myocarditis. We also conclude that blocking α7nAchR reduces the phosphorylation of STAT3, increases the expression of TNF-α and IL-6, aggravating viral myocarditis.

Indexed as

Aconitinealpha7 Nicotinic Acetylcholine ReceptorAnimalsAnti-Inflammatory AgentsCytokinesEnterovirus B, HumanGene Expression RegulationInterleukin-6MiceMice, Inbred BALB CMyocarditisNicotineSignal TransductionSTAT3 Transcription FactorSurvival AnalysisTumor Necrosis Factor-alphaAconitinealpha7 Nicotinic Acetylcholine ReceptorAnti-Inflammatory AgentsCytokinesInterleukin-6methyllycaconitineNicotineSTAT3 Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID25396421
PMCPMC4232511
OpenAlexW2034835379

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.