Evidence map›Paper›PMID 25768281›Full record

ArticlePloS one2015

A DPP-4 inhibitor suppresses fibrosis and inflammation on experimental autoimmune myocarditis in mice.

Hiroyuki Hirakawa, Hirofumi Zempo, Masahito Ogawa, Ryo Watanabe, Jun-Ichi Suzuki, Hiroshi Akazawa, Issei Komuro, Mitsuaki Isobe

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
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  6. Review
  7. Review
  8. Article
  9. Modulation of TLR4/NFκB Pathways in Autoimmune Myocarditis.Antioxidants (Basel, Switzerland) · 2023
    Article
  10. Article
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  12. Review
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  16. Article
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  19. Article
  20. Sitagliptin Inhibits Extracellular Matrix Accumulation and Proliferation in Lung Fibroblasts.Medical science monitor : international medical journal of experimental and clinical research · 2020
    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

8 authors at 2 institutions in 1 country.

Hiroyuki HirakawaDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Hirofumi ZempoDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Masahito OgawaDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Ryo WatanabeDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Jun-Ichi SuzukiDepartment of Advanced Clinical Science and Therapeutics, The University of Tokyo, Tokyo, Japan.
Hiroshi AkazawaDepartment of Advanced Clinical Science and Therapeutics, The University of Tokyo, Tokyo, Japan.
Issei KomuroDepartment of Cardiovascular Medicine, The University of Tokyo, Tokyo, Japan.
Mitsuaki IsobeDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Tokyo Medical and Dental University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocarditis is a critical inflammatory disorder which causes life-threatening conditions. No specific or effective treatment has been established. DPP-4 inhibitors have salutary effects not only on type 2 diabetes but also on certain cardiovascular diseases. However, the role of a DPP-4 inhibitor on myocarditis has not been investigated. To clarify the effects of a DPP-4 inhibitor on myocarditis, we used an experimental autoimmune myocarditis (EAM) model in Balb/c mice. EAM mice were assigned to the following groups: EAM mice group treated with a DPP-4 inhibitor (linagliptin) (n = 19) and those untreated (n = 22). Pathological analysis revealed that the myocardial fibrosis area ratio in the treated group was significantly lower than in the untreated group. RT-PCR analysis demonstrated that the levels of mRNA expression of IL-2, TNF-α, IL-1β and IL-6 were significantly lower in the treated group than in the untreated group. Lymphocyte proliferation assay showed that treatment with the DPP-4 inhibitor had no effect on antigen-induced spleen cell proliferation. Administration of the DPP-4 inhibitor remarkably suppressed cardiac fibrosis and reduced inflammatory cytokine gene expression in EAM mice. Thus, the agents present in DPP-4 inhibitors may be useful to treat and/or prevent clinical myocarditis.

Indexed as

AnimalsAutoimmune DiseasesCell ProliferationDipeptidyl-Peptidase IV InhibitorsDisease Models, AnimalFibrosisHeartHeart Function TestsInflammationLinagliptinLungLymphocytesMaleMiceMice, Inbred BALB CMyocarditisDipeptidyl-Peptidase IV InhibitorsLinagliptin

Identifiers

PMID25768281
PMCPMC4359137
OpenAlexW1994583005

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.