Evidence map›Paper›PMID 34083516›Full record

ArticleCell death & disease2021

IL-37b alleviates endothelial cell apoptosis and inflammation in Kawasaki disease through IL-1R8 pathway.

Chang Jia, Yingzhi Zhuge, Shuchi Zhang, Chao Ni, Linlin Wang, Rongzhou Wu, Chao Niu, Zhengwang Wen, Xing Rong, Huixian Qiu and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
10.9field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 63 citations in OpenAlex.

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  10. SIGIRR: An Orphan Receptor Mediating Anti-inflammatory Actions.Expert reviews in molecular medicine · 2025
    Review
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  16. [Role and mechanisms of CHI3L1 in coronary artery lesions in a mouse model of Kawasaki disease-like vasculitis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Chang Jia *Pediatric Research Institute, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Yingzhi Zhuge *Children's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Shuchi ZhangChildren's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Chao NiChildren's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Linlin WangChildren's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Rongzhou WuChildren's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Chao NiuPediatric Research Institute, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Zhengwang WenChildren's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Xing RongChildren's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China.
Huixian QiuChildren's Heart Center, Institute of Cardiovascular Development and Translational Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China. qiuhx1053@126.com.
Maoping ChuPediatric Research Institute, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, China. chmping@hotmail.com.ORCID http://orcid.org/0000-0003-0975-7176
Wenzhou Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81900240National Natural Science Foundation of China (National Science Foundation of China) 81970435, 81770502National Natural Science Foundation of China (National Science Foundation of China) 82000469Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LY18H020012
6 · The paper itself

Abstract

Kawasaki disease (KD) is an acute vasculitis of pediatric populations that may develop coronary artery aneurysms if untreated. It has been regarded as the principal cause of acquired heart disease in children of the developed countries. Interleukin (IL)-37, as one of the IL-1 family members, is a natural suppressor of inflammation that is caused by activation of innate and adaptive immunity. However, detailed roles of IL-37 in KD are largely unclear. Sera from patients with KD displayed that IL-37 level was significantly decreased compared with healthy controls (HCs). QRT-PCR and western blot analyses showed that the expression level of IL-37 variant, IL-37b, was remarkably downregulated in human umbilical vein endothelial cells (HUVECs) exposed to KD sera-treated THP1 cells. Therefore, we researched the role of IL-37b in the context of KD and hypothesized that IL-37b may have a powerful protective effect in KD patients. We first observed and substantiated the protective role of IL-37b in a mouse model of KD induced by Candida albicans cell wall extracts (CAWS). In vitro experiments demonstrated that IL-37b alleviated endothelial cell apoptosis and inflammation via IL-1R8 receptor by inhibiting ERK and NFκB activation, which were also recapitulated in the KD mouse model. Together, our findings suggest that IL-37b play an effective protective role in coronary endothelial damage in KD, providing new evidence that IL-37b is a potential candidate drug to treat KD.

Indexed as

AnimalsApoptosisDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsInflammationInterleukin-1MaleMiceMice, Inbred C57BLMucocutaneous Lymph Node SyndromeReceptors, Interleukin-1Signal TransductionIL37 protein, humanInterleukin-1Receptors, Interleukin-1SIGIRR protein, humanSIGIRR protein, mouse

Identifiers

PMID34083516
PMCPMC8174541
OpenAlexW3164098369

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.