Evidence map›Paper›PMID 31746138›Full record

ArticleJournal of cellular and molecular medicine2020

Interleukin-38 alleviates cardiac remodelling after myocardial infarction.

Yuzhen Wei, Yin Lan, Yucheng Zhong, Kunwu Yu, Wenbin Xu, Ruirui Zhu, Haitao Sun, Yan Ding, Yue Wang, Qiutang Zeng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.9field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  13. Interleukin-38 and Insulin Resistance.Endocrine, metabolic & immune disorders drug targets · 2024
    Article
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  15. The emerging role of IL-38 in diseases: A comprehensive review.Immunity, inflammation and disease · 2023
    Review
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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 1 institution in 1 country.

Yuzhen WeiInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Yin LanInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Yucheng ZhongInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Kunwu YuInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Wenbin XuInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Ruirui ZhuInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Haitao SunInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Yan DingInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Yue WangInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Qiutang ZengInstitute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.ORCID 0000-0002-2192-3635
Wuhan Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive immune-mediated inflammatory reaction plays a deleterious role in ventricular remodelling after myocardial infarction (MI). Interleukin (IL)-38 is a newly characterized cytokine of the IL-1 family and has been reported to exert a protective effect in some autoimmune diseases. However, its role in cardiac remodelling post-MI remains unknown. In this study, we found that the expression of IL-38 was increased in infarcted heart after MI induced in C57BL/6 mice by permanent ligation of the left anterior descending artery. In addition, our data showed that ventricular remodelling after MI was significantly ameliorated after recombinant IL-38 injection in mice. This amelioration was demonstrated by better cardiac function, restricted inflammatory response, attenuated myocardial injury and decreased myocardial fibrosis. Our results in vitro revealed that IL-38 affects the phenotype of dendritic cells (DCs) and IL-38 plus troponin I (TNI)-treated tolerogenic DCs dampened adaptive immune response when co-cultured with CD4

Indexed as

Ventricular RemodelingAnimalsApoptosisDendritic CellsFibrosisImmune ToleranceInflammationInterleukin-1MaleMice, Inbred C57BLMyocardial InfarctionMyocytes, CardiacPhenotypeRNA, MessengerSurvival AnalysisT-Lymphocytes, RegulatoryIl1f10 protein, mouseInterleukin-1RNA, MessengerTroponin Icardiac remodellinginflammationinterleukin-38myocardial infarction

Identifiers

PMID31746138
PMCPMC6933378
OpenAlexW2990336235

What OpenQuestion holds

Textmetadata
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.