Evidence map›Paper›PMID 25089642›Full record

ArticleAnesthesiology2014

Role of cardiac- and myeloid-MyD88 signaling in endotoxin shock: a study with tissue-specific deletion models.

Yan Feng, Lin Zou, Chan Chen, Dan Li, Wei Chao

Open access · bronzeAbstract read
In one paragraph

Article in Anesthesiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 39% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

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  19. Overexpression of myeloid differentiation protein 88 in mice induces mild cardiac dysfunction, but no deficit in heart morphology.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016
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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

5 authors at 1 institution in 2 countries.

Yan FengFrom the Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Lin Zou
Chan Chen
Dan Li
Wei Chao
School of the Art Institute of Chicago · US

Funding

Role of TLR-cfB Signaling in SepsisR01GM097259 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI CHAO, WEI · 2012 to 2015
$1.9M
Role of Toll-like Receptor 4 (TLR4) in Ischemic Myocardial InjuryR01GM080906 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI CHAO, WEI · 2007 to 2011
$1.6M
NIGMS NIH HHS R01 GM080906NIGMS NIH HHS R01-GM080906NIGMS NIH HHS R01 GM097259NIGMS NIH HHS R01-GM097259
6 · The paper itself

Abstract

backgroundMyeloid differentiation factor 88 (MyD88) is an adaptor molecule critical for host innate immunity. Studies have shown that signaling via MyD88 contributes to cytokine storm, cardiac dysfunction, and high mortality during endotoxin shock.However, the specific contribution of MyD88 signaling of immune and cardiac origins to endotoxin shock remains unknown.

methodsTissue-specific MyD88 deletion models: Cre-recombinase transgenic mice with α-myosin heavy chain (α-MHC) or lysozyme M promoters were cross-bred with MyD88-loxP (MyD88fl/fl) mice, respectively, to generate cardiomyocyte- (α-MHCMyD88−/−) or myeloid-specific (Lyz-MyD88−/−) MyD88 deletion models and their respective MyD88fl/fl littermates. Endotoxin shock model: Mice were subjected to 15 mg/kg lipopolysaccharide (intraperitoneal injection). Cardiac function was measured by echocardiography and cytokines by multiplex assay and quantitative reverse transcription-polymerase chain reaction.

resultsα-MHC-MyD88−/− mice had 61 and 87% reduction in MyD88 gene and protein expression in cardiomyocytes,respectively, whereas Lyz-MyD88−/− had 73 and 67% decrease, respectively, in macrophages (n=3 per group). After lipopolysaccharide treatment, the two groups of MyD88fl/fl littermates had 46% (n=10) and 60% (n=15) of mortality, respectively.Both α-MHC-MyD88−/− and Lyz-MyD88−/− mice had markedly improved survival. Compared with the MyD88fl/fl littermates, Lyz-MyD88−/− mice had warmer body temperature, attenuated systemic and cardiac inflammatory cytokine production,and significantly improved cardiac function, whereas α-MHC-MyD88−/− mice had decreased myocardial inducible nitricoxide synthase induction and modestly preserved cardiac function.

conclusionsBoth cardiomyocyte- and myeloid-MyD88 signaling play a role in cardiac dysfunction and mortality during endotoxin shock. Myeloid-MyD88 signaling plays a predominant role in systemic and cardiac inflammation after endotoxin challenge.

Indexed as

Stem CellsAnimalsBody TemperatureGene DeletionHeartMacrophagesMice, KnockoutMice, TransgenicMyeloid Differentiation Factor 88Myocytes, CardiacShock, SepticSignal TransductionUltrasonographyMyd88 protein, mouseMyeloid Differentiation Factor 88

Identifiers

PMID25089642
PMCPMC4237623
OpenAlexW2010120262

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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.