Evidence map›Paper›PMID 19151078›Full record

ArticleEuropean journal of heart failure2009

Suppression of inflammation in rat autoimmune myocarditis by S100A8/A9 through modulation of the proinflammatory cytokine network.

Kaoru Otsuka, Fumio Terasaki, Masaki Ikemoto, Shuichi Fujita, Bin Tsukada, Takashi Katashima, Yumiko Kanzaki, Koichi Sohmiya, Tatsuji Kono, Haruhiro Toko and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in European journal of heart failure, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Hyperbaric Oxygen Therapy in Experimental Autoimmune Myocarditis: Insights from Preclinical Models to Translational Perspectives.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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  10. S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023
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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

12 authors at 3 institutions in 1 country.

Kaoru OtsukaDepartment of Internal Medicine III, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki 569-8686, Japan.
Fumio Terasaki
Masaki Ikemoto
Shuichi Fujita
Bin Tsukada
Takashi Katashima
Yumiko Kanzaki
Koichi Sohmiya
Tatsuji Kono
Haruhiro Toko
Masatoshi Fujita
Yasushi Kitaura
Osaka Medical and Pharmaceutical University · JPKyoto University · JPChiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsS100A8/A9 is expressed in activated monocytes/macrophages and assumed to be heavily involved in the pathogenesis of acute inflammation. Although several studies have asserted that S100A8/A9 has a proinflammatory function, the exact biological function of S100A8/A9 is yet to be described. We examined the anti-inflammatory effects of S100A8/A9 on experimental autoimmune myocarditis (EAM) in rats. METHODS AND

resultsExperimental autoimmune myocarditis was induced in Lewis rats by immunization with porcine cardiac myosin. The recombinant (R-) S100A8/A9 was injected intraperitoneally into EAM rats. R-S100A8/A9 attenuated the severity of myocarditis, as evidenced by echocardiographic and histological findings. In addition, we found that not only the mRNA expression of proinflammatory cytokines [interleukin (IL)-1beta, IL-6, and tumour necrosis factor (TNF)-alpha] in the myocardium, but also their serum concentrations were suppressed in EAM rats treated with R-S100A8/A9. Nuclear factor-kappa B expression in inflammatory cells was also suppressed in the treated rats. To elucidate the mechanistic function of S100A8/A9 on proinflammatory cytokines in vivo, we used an ELISA on the supernatant of homogenized heart tissue treated with R-S100A8/A9. The findings revealed high-affinity binding of R-S100A8/A9 with IL-1beta, IL-6, and TNF-alpha in the myocardium, suggesting the trapping of proinflammatory cytokines by R-S100A8/A9.

conclusionS100A8/A9 attenuates EAM through modulation of the proinflammatory cytokine network.

Indexed as

AnimalsAutoimmune DiseasesCalgranulin ACytokinesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayMacrophagesMaleMyocarditisMyocardiumRatsRats, Inbred LewRecombinant ProteinsRNA, MessengerTreatment OutcomeCalgranulin ACytokinesRecombinant ProteinsRNA, Messenger

Identifiers

PMID19151078
PMCPMC2645050
OpenAlexW2024400965

What OpenQuestion holds

Textmetadata
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.