Evidence map›Paper›PMID 36289897›Full record

ArticleBiomedicines2022

Inhibition of TRIF-Dependent Inflammation Decelerates Afterload-Induced Myocardial Remodeling.

Stephanie I Bettink, Jan-Christian Reil, Andrey Kazakov, Christina Körbel, Dominic Millenaar, Ulrich Laufs, Bruno Scheller, Michael Böhm, Stephan H Schirmer

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

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

9 authors at 3 institutions in 1 country.

Stephanie I BettinkInternal Medicine III, Saarland University, 66421 Homburg, Germany.ORCID 0000-0003-0865-5047
Jan-Christian ReilMedical Clinic II, University Hospital Schleswig-Holstein, 23538 Lübeck, Germany.
Andrey KazakovInternal Medicine III, Saarland University, 66421 Homburg, Germany.
Christina KörbelInstitute for Clinical & Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Dominic MillenaarInternal Medicine III, Saarland University, 66421 Homburg, Germany.
Ulrich LaufsDepartment of Cardiology, Leipzig University, 04103 Leipzig, Germany.
Bruno SchellerInternal Medicine III, Saarland University, 66421 Homburg, Germany.
Michael BöhmInternal Medicine III, Saarland University, 66421 Homburg, Germany.
Stephan H SchirmerInternal Medicine III, Saarland University, 66421 Homburg, Germany.
Saarland University · DELeipzig University · DEUniversity Hospital Schleswig-Holstein · DE

Funding

Deutsche Forschungsgemeinschaft KFO196Deutsche Forschungsgemeinschaft TTR219Saarland University HOMFOR
6 · The paper itself

Abstract

Pressure-overload-induced cardiac hypertrophy represents one cause of the development of heart failure. The aim of this study is to characterize the influence of the TIR-domain-containing adapter-inducing interferon-β (TRIF) during afterload-induced myocardial remodeling. After trans-aortic constriction (TAC), cardiac pressure overload leads to an early increase in MyD88- (Myeloid differentiation primary response gene 88) and TRIF-dependent cytokines. The maximum cytokine expression appeared within the first week and decreased to its control level within five weeks. While cardiomyocyte hypertrophy was comparable, the myocardial accumulation of the inflammatory cells was lower in TRIF

Indexed as

afterloadfibrosishypertrophyinflammationTRIF

Identifiers

PMID36289897
PMCPMC9599817
OpenAlexW4306836290

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.