Evidence map›Paper›PMID 30460984›Full record

ArticleBritish journal of pharmacology2019

Exogenous IL-19 attenuates acute ischaemic injury and improves survival in male mice with myocardial infarction.

Weishuai An, Yongsheng Yu, Yuefan Zhang, Zhigang Zhang, Yunhua Yu, Xianxian Zhao

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Role of post-translational modifications of Sp1 in cardiovascular diseases.Frontiers in cell and developmental biology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Resolution of inflammation in immune and nonimmune cells by interleukin-19.American journal of physiology. Cell physiology · 2020
    Review
  11. Observational
  12. Review
  13. 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

6 authors at 4 institutions in 1 country.

Weishuai AnDepartment of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.
Yongsheng YuDepartment of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.
Yuefan ZhangDepartment of Clinical Pharmacy, Shanghai General Hospital, Shanghai Jiaotong University, Shanghai, China.
Zhigang ZhangDepartment of Cardiology, Putuo Center Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Yunhua YuDepartment of Geriatrics, Fuzhou General Hospital, Fujian Medical University, Fuzhou, China.
Xianxian ZhaoDepartment of Cardiovasology, Changhai Hospital, Second Military Medical University, Shanghai, China.ORCID 0000-0002-0648-3897
Fujian Medical University · CNSecond Military Medical University · CNShanghai Jiao Tong University · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeMyocardial infarction (MI) is one of the leading causes of death in China and often results in the development of heart failure. In this work, we tested the therapeutic role of Interleukin-19 (IL-19) in mice with MI and investigated the underlying molecular mechanism. EXPERIMENTAL APPROACH: Mice were subjected to MI by ligation of left anterior descending coronary artery (LAD) and treated with IL-19 (10ng g KEY

resultsProtein expression of IL-19 and its receptor in myocardium were upregulated 24 hrs post-MI in male mice. IL-19 treatment decreased infarct and apoptosis in myocardium, accompanied by enhanced haem oxygenase-1 (HO-1) activities and reduced malondialdehyde (MDA) formation. Pretreatment with IL-19 upregulated HO-1 expression in cultured neonatal mouse ventricular myocytes and attenuated oxygen-glucose deprivation (OGD)-induced injuries in vitro. Furthermore, IL-19 preserved cardiac function and improved survival of mice with MI. IL-19 reduced inflammatory infiltrates and suppressed formation of TNF-α, IL-1β, and IL-6. More importantly, IL-19 inhibited polarization toward proinflammatory M1 macrophages and stimulated M2 macrophage polarization in myocardium of mice with MI. IL-19 enhanced protein levels of vascular endothelial growth factor (VEGF) and promoted angiogenesis in myocardium of mice with MI. In addition, IL-19 treatment increased DNA-binding of the transcription factor STAT3 in myocardium of mice with MI. CONCLUSIONS AND IMPLICATIONS: Treatment with exogenous IL-19 attenuated acute ischemic injury and improved survival of mice with MI. The mechanisms underlying these effects involved induction of HO-1, M2 macrophage polarization, angiogenesis, and STAT3 activation.

Indexed as

AnimalsCells, CulturedCoronary VesselsCytokinesHeartHeme Oxygenase-1Macrophage ActivationMaleMembrane ProteinsMice, Inbred C57BLMyocardial InfarctionMyocardiumNeovascularization, PhysiologicReceptors, InterleukinSTAT3 Transcription FactorVascular Endothelial Growth Factor ACytokinesHeme Oxygenase-1Hmox1 protein, mouseMembrane ProteinsReceptors, InterleukinStat3 protein, mouseSTAT3 Transcription FactorVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID30460984
PMCPMC6365357
OpenAlexW2901187962

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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.