Evidence map›Paper›PMID 31552054›Full record

ArticleFrontiers in immunology2019

Bruton's Tyrosine Kinase Inhibition Attenuates the Cardiac Dysfunction Caused by Cecal Ligation and Puncture in Mice.

Caroline E O'Riordan, Gareth S D Purvis, Debora Collotta, Fausto Chiazza, Bianka Wissuwa, Sura Al Zoubi, Lara Stiehler, Lukas Martin, Sina M Coldewey, Massimo Collino and 1 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. [Recent research on pyroptosis in sepsis-induced myocardial depression].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
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  20. Targeting the NLRP3 Inflammasome via BTK.Frontiers in cell and developmental biology · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 3 countries.

Caroline E O'RiordanWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Gareth S D PurvisWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Debora CollottaDepartment of Drug Science and Technology, University of Turin, Turin, Italy.
Fausto ChiazzaDepartment of Drug Science and Technology, University of Turin, Turin, Italy.
Bianka WissuwaDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Sura Al ZoubiWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Lara StiehlerWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Lukas MartinWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Sina M ColdeweyDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Massimo CollinoDepartment of Drug Science and Technology, University of Turin, Turin, Italy.
Christoph ThiemermannWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
University of Turin · ITWilliam Harvey Research Institute · GBJena University Hospital · DEUniversitätsklinikum Aachen · DEQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is one of the most prevalent diseases in the world. The development of cardiac dysfunction in sepsis results in an increase of mortality. It is known that Bruton's tyrosine kinase (BTK) plays a role in toll-like receptor signaling and NLRP3 inflammasome activation, two key components in the pathophysiology of sepsis and sepsis-associated cardiac dysfunction. In this study we investigated whether pharmacological inhibition of BTK (ibrutinib 30 mg/kg and acalabrutinib 3 mg/kg) attenuates sepsis associated cardiac dysfunction in mice. 10-week old male C57BL/6 mice underwent CLP or sham surgery. One hour after surgery mice received either vehicle (5% DMSO + 30% cyclodextrin i.v.), ibrutinib (30 mg/kg i.v.), or acalabrutinib (3 mg/kg i.v.). Mice also received antibiotics and an analgesic at 6 and 18 h. After 24 h, cardiac function was assessed by echocardiography

Indexed as

AdenineAgammaglobulinaemia Tyrosine KinaseAnimalsBenzamidesCecumDisease Models, AnimalHeartHeart DiseasesInflammasomesLigationMaleMiceMice, Inbred C57BLPiperidinesProtein Kinase InhibitorsPuncturesacalabrutinibAdenineAgammaglobulinaemia Tyrosine KinaseBenzamidesibrutinibInflammasomesPiperidinesProtein Kinase InhibitorsPyrazinesPyrazolesPyrimidinesacalabrutinibBruton's tyrosine kinase (BTK)cardiac dysfunctionibrutinibmiceNF-κBNLRP3sepsis

Identifiers

PMID31552054
PMCPMC6743418
OpenAlexW2969789732

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.