Evidence map›Paper›PMID 28640392›Full record

ArticleClinical and experimental immunology2017

Calcineurin inhibitors exacerbate coronary arteritis via the MyD88 signalling pathway in a murine model of Kawasaki disease.

K Murata, Y Motomura, T Tanaka, S Kanno, T Yano, M Onimaru, A Shimoyama, H Nishio, Y Sakai, M Oh-Hora and 7 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Protein phosphatases in TLR signaling.Cell communication and signaling : CCS · 2021
    Review
  3. Article
  4. Review
  5. Refractory Kawasaki disease: diagnostic and management challenges.Pediatric health, medicine and therapeutics · 2019
    Review
  6. Kawasaki Disease.Frontiers in pediatrics · 2018
    Review
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

17 authors at 4 institutions in 1 country.

K MurataDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID 0000-0002-2698-7160
Y MotomuraDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
T TanakaDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
S KannoDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
T YanoDepartment of Pharmacy, Kyushu University Hospital, Fukuoka, Japan.
M OnimaruDivision of Pathophysiological and Experimental Pathology, Department of Pathology, Kyushu University, Fukuoka, Japan.
A ShimoyamaDepartment of Chemistry, Graduate School of Science, Osaka University, Osaka, Japan.
H NishioDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Y SakaiDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
M Oh-HoraDivision of Molecular Immunology, Research Center for Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
H HaraDepartment of Immunology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
K FukaseDepartment of Chemistry, Graduate School of Science, Osaka University, Osaka, Japan.
H TakadaDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
S MasudaDepartment of Pharmacy, Kyushu University Hospital, Fukuoka, Japan.
S OhgaDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
S YamasakiDivision of Molecular Immunology, Research Center for Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
T HaraDivision of Molecular Immunology, Research Center for Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Kyushu University · JPKyushu University Hospital · JPThe University of Osaka · JPKagoshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcineurin inhibitors (CNIs) have been used off-label for the treatment of refractory Kawasaki disease (KD). However, it remains unknown whether CNIs show protective effects against the development of coronary artery lesions in KD patients. To investigate the effects of CNIs on coronary arteries and the mechanisms of their actions on coronary arteritis in a mouse model of KD, we performed experiments with FK565, a ligand of nucleotide-binding oligomerization domain-containing protein 1 (NOD1) in wild-type, severe combined immunodeficiency (SCID), caspase-associated recruitment domain 9 (CARD9)

Indexed as

AnimalsArteritisCalcineurin InhibitorsCARD Signaling Adaptor ProteinsCoronary VesselsCytokinesDisease Models, AnimalEndothelium, VascularHumansInflammation MediatorsMacrophagesMiceMice, Inbred C57BLMice, KnockoutMice, SCIDMucocutaneous Lymph Node SyndromeCalcineurin InhibitorsCard9 protein, mouseCARD Signaling Adaptor ProteinsCytokinesheptanoyl-gamma-D-glutamyl-L-meso-diaminopimelyl-D-alanineInflammation MediatorsMyeloid Differentiation Factor 88Oligopeptidescalcineurin inhibitorscoronary arteritisKawasaki diseasemouse modelMyD88

Identifiers

PMID28640392
PMCPMC5588765
OpenAlexW2645692333

What OpenQuestion holds

Textmetadata
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.