Evidence map›Paper›PMID 38457368›Full record

ArticleClinical and experimental immunology2024

α2-Antiplasmin is associated with macrophage activation and fibrin deposition in a macrophage activation syndrome mouse model.

Yosuke Kanno, Kinomi Toyama, Haruna Shibata, Osamu Matsuo, Kei-Ichi Ozaki

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

Article in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

5 authors at 2 institutions in 1 country.

Yosuke KannoDepartment of Molecular Pathology, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kodo Kyo-tanabe, Kyoto, Japan.ORCID 0000-0001-9741-2113
Kinomi ToyamaDepartment of Molecular Pathology, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kodo Kyo-tanabe, Kyoto, Japan.
Haruna ShibataDepartment of Molecular Pathology, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kodo Kyo-tanabe, Kyoto, Japan.
Osamu MatsuoFaculty of Medicine, Kindai University, Osaka-sayama, Japan.
Kei-Ichi OzakiDepartment of Molecular Pathology, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kodo Kyo-tanabe, Kyoto, Japan.
Doshisha Women's College of Liberal Arts · JPKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage activation syndrome (MAS) is a life-threatening condition, characterized by cytopenia, multi-organ dysfunction, and coagulopathy associated with excessive activation of macrophages. In this study, we investigated the roles of alpha2-antiplasmin (α2AP) in the progression of MAS using fulminant MAS mouse model induced by toll-like receptor-9 agonist (CpG) and D-(+)-galactosamine hydrochloride (DG). α2AP deficiency attenuated macrophage accumulation, liver injury, and fibrin deposition in the MAS model mice. Interferon-γ (IFN-γ) is associated with macrophage activation, including migration, and plays a pivotal role in MAS progression. α2AP enhanced the IFN-γ-induced migration, and tissue factor production. Additionally, we showed that fibrin-induced macrophage activation and tumor necrosis factor-α production. Moreover, the blockade of α2AP by neutralizing antibodies attenuated macrophage accumulation, liver injury, and fibrin deposition in the MAS model mice. These data suggest that α2AP may regulate IFN-γ-induced responses and be associated with macrophage activation and fibrin deposition in the MAS progression.

Indexed as

alpha-2-AntiplasminFibrinMacrophage ActivationMacrophage Activation SyndromeMacrophagesAnimalsDisease Models, AnimalGalactosamineInterferon-gammaLiverMaleMiceMice, Inbred C57BLMice, KnockoutTumor Necrosis Factor-alphaalpha-2-AntiplasminFibrinGalactosamineInterferon-gammaTumor Necrosis Factor-alphachemotaxis/migrationinflammationmacrophage

Identifiers

PMID38457368
PMCPMC11097911
OpenAlexW4392626974

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.