Evidence map›Paper›PMID 28920098›Full record

ArticleJACC. Basic to translational science2017

The IL-1RI Co-Receptor TILRR (

Sarah A Smith, Andriy O Samokhin, Mabruka Alfadi, Emer C Murphy, David Rhodes, W Mike L Holcombe, Endre Kiss-Toth, Robert F Storey, Siu-Pok Yee, Sheila E Francis and 1 more

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Article
  7. Article
  8. Agent-Based Modeling of Complex Molecular Systems.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  9. Integrated Bioinformatics IdentifiesApplied bionics and biomechanics · 2022
    Article
  10. TILRR Aggravates Sepsis-Induced Acute Lung Injury by Suppressing the PI3K/Akt Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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

11 authors at 2 institutions in 2 countries.

Sarah A SmithDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Andriy O SamokhinDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Mabruka AlfadiDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Emer C MurphyDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
David RhodesDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
W Mike L HolcombeDepartment of Computer Science, University of Sheffield, Sheffield, United Kingdom.
Endre Kiss-TothDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Robert F StoreyDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Siu-Pok YeeDepartment of Cell Biology, University of Connecticut, Farmington, Connecticut.
Sheila E FrancisDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Eva E QwarnstromDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
University of Sheffield · GBUniversity of Connecticut · US

Funding

British Heart Foundation PG/11/103/29219
6 · The paper itself

Abstract

Expression of the interleukin-1 receptor type I (IL-1RI) co-receptor Toll-like and interleukin-1 receptor regulator (TILRR) is significantly increased in blood monocytes following myocardial infarction and in the atherosclerotic plaque, whereas levels in healthy tissue are low. TILRR association with IL-1RI at these sites causes aberrant activation of inflammatory genes, which underlie progression of cardiovascular disease. The authors show that genetic deletion of TILRR or antibody blocking of TILRR function reduces development of atherosclerotic plaques. Lesions exhibit decreased levels of monocytes, with increases in collagen and smooth muscle cells, characteristic features of stable plaques. The results suggest that TILRR may constitute a rational target for site- and signal-specific inhibition of vascular disease.

Indexed as

ApoE, apolipoprotein EDK, double knockoutGAPDH, glyceraldehyde 3-phosphate dehydrogenaseheparan sulfate proteoglycaniBALT, inducible bronchus-associated lymphoid tissueIgG, immunoglobulin GIL-1RIIL-1RI, interleukin-1 receptor type IIL, interleukininterleukin-1 receptorIκBα, inhibitor kappa B alphaKO, knockoutLDLR–/–, low-density lipoprotein receptor–/–LPS, lipopolysaccharideNF-κBNF-κB, nuclear factor-kappa BNSTEMI, non–ST-segment elevation myocardial infarctionPBS, phosphate-buffered salinePCR, polymerase chain reactionqPCR, quantitative polymerase chain reactionSDS, sodium dodecyl sulfateSTEMI, ST-segment elevation myocardial infarctionTILRRTILRR, toll-like and interleukin-1 receptor regulator

Identifiers

PMID28920098
PMCPMC5582195
OpenAlexW2745913172

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.