Evidence map›Paper›PMID 19505385›Full record

ArticleInternational journal of immunopathology and pharmacology

Inflammasomes are differentially expressed in cardiovascular and other tissues.

Y Yin, Y Yan, X Jiang, J Mai, N C Chen, H Wang, X-F Yang

Open access · greenAbstract read
In one paragraph

Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

115 citing papers in PubMed, 174 citations in OpenAlex.

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  7. Innate and adaptive immunity in acute myocarditis.International journal of cardiology · 2024
    Review
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  16. The inflammasomes: crosstalk between innate immunity and hematology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  17. Article
  18. Review
  19. Review
  20. Article

55 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Y YinDepartment of Pharmacology and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, USA.
Y Yan
X Jiang
J Mai
N C Chen
H Wang
X-F Yang
Temple University · US

Funding

Suppression of vascular endothelial cell inflammationR01HL094451 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2009 to 2013
$1.8M
NHLBI NIH HHS R01 HL094451
6 · The paper itself

Abstract

To determine the expression of components in Toll-like receptors (TLRs)/Nod-like receptors (NLRs)/inflammasome/caspase-1/interleukin (IL-1)-beta pathway, we examined the expression profiles of those genes by analyzing the data from expression sequence tag cDNA cloning and sequencing. We made several important findings: firstly, among 11 tissues examined, vascular tissues and heart express fewer types of TLRs and NLRs than immune and defense tissues including blood, lymph nodes, thymus and trachea; secondly, brain, lymph nodes and thymus do not express proinflammatory cytokines IL-1beta and IL-18 constitutively, suggesting that these two cytokines need to be upregulated in the tissues; and thirdly, based on the expression data of three characterized inflammasomes (NALP1, NALP3 and IPAF inflammasome), the examined tissues can be classified into three tiers: the first tier tissues including brain, placenta, blood and thymus express inflammasome(s) in constitutive status; the second tier tissues have inflammasome(s) in nearly-ready expression status (with the requirement of upregulation of one component); the third tier tissues, like heart and bone marrow, require upregulation of at least two components in order to assemble functional inflammasomes. Our original model of three-tier expression of inflammasomes would suggest a new concept of tissue inflammation privilege, and provides an insight to the differences among tissues in initiating acute inflammation in response to stimuli.

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCalcium-Binding ProteinsCardiovascular SystemCARD Signaling Adaptor ProteinsCarrier ProteinsCells, CulturedEndothelial CellsGene Expression ProfilingGene Expression RegulationHumansInflammationInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsInterleukin-18Interleukin-1betaNLRC4 protein, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP1 protein, humanNLRP3 protein, humanNLR ProteinsNod Signaling Adaptor ProteinsToll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID19505385
PMCPMC2847797
OpenAlexW1886716828

What OpenQuestion holds

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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.