Evidence map›Paper›PMID 24791857›Full record

ArticleLeukemia2015

Inhibition of plasmin attenuates murine acute graft-versus-host disease mortality by suppressing the matrix metalloproteinase-9-dependent inflammatory cytokine storm and effector cell trafficking.

A Sato, C Nishida, K Sato-Kusubata, M Ishihara, Y Tashiro, I Gritli, H Shimazu, S Munakata, H Yagita, K Okumura and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 53 citations in OpenAlex.

  1. Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025
    Review
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  14. Nrf2 Activator PB125Antioxidants (Basel, Switzerland) · 2020
    Article
  15. Article
  16. Article
  17. Review
  18. Proteomic Characterization Reveals That MMP-3 Correlates With Bronchiolitis Obliterans Syndrome Following Allogeneic Hematopoietic Cell and Lung Transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016
    Article
  19. 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

17 authors at 3 institutions in 1 country.

A SatoDepartment of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
C Nishida1] Department of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan [2] Department of Stem Cell Dynamics, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
K Sato-KusubataDepartment of Stem Cell Dynamics, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
M IshiharaDepartment of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
Y TashiroDepartment of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
I GritliDepartment of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
H ShimazuDepartment of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
S MunakataDepartment of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan.
H YagitaDepartment of Immunology, Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, Japan.
K OkumuraDepartment of Immunology, Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, Japan.
Y TsudaFaculty of Pharmaceutical Sciences, Kobe Gakuin University, Kobe, Japan.
Y OkadaFaculty of Pharmaceutical Sciences, Kobe Gakuin University, Kobe, Japan.
A TojoDepartment of Hematology and Oncology, Center for Stem Cell Biology and Regenerative Medicine, Tokyo, Japan.
H NakauchiDepartment of Hematology and Oncology, Center for Stem Cell Biology and Regenerative Medicine, Tokyo, Japan.
S TakahashiDepartment of Hematology and Oncology, Center for Stem Cell Biology and Regenerative Medicine, Tokyo, Japan.
B Heissig1] Department of Stem Cell Dynamics, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan [2] Department of Immunology, Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, Japan.
K Hattori1] Department of Stem Cell Regulation, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science at the University of Tokyo (IMSUT), Tokyo, Japan [2] Department of Immunology, Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, Japan.
The University of Tokyo · JPJuntendo University · JPKobe Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The systemic inflammatory response observed during acute graft-versus-host disease (aGVHD) is driven by proinflammatory cytokines, a 'cytokine storm'. The function of plasmin in regulating the inflammatory response is not fully understood, and its role in the development of aGVHD remains unresolved. Here we show that plasmin is activated during the early phase of aGVHD in mice, and its activation correlated with aGVHD severity in humans. Pharmacological plasmin inhibition protected against aGVHD-associated lethality in mice. Mechanistically, plasmin inhibition impaired the infiltration of inflammatory cells, the release of membrane-associated proinflammatory cytokines including tumor necrosis factor-α (TNF-α) and Fas-ligand directly, or indirectly via matrix metalloproteinases (MMPs) and alters monocyte chemoattractant protein-1 (MCP-1) signaling. We propose that plasmin and potentially MMP-9 inhibition offers a novel therapeutic strategy to control the deadly cytokine storm in patients with aGVHD, thereby preventing tissue destruction.

Indexed as

AnimalsBase SequenceBiological TransportCell LineDisease Models, AnimalDNA PrimersEnzyme-Linked Immunosorbent AssayFemaleFibrinolysinGraft vs Host DiseaseHumansInflammation MediatorsMatrix Metalloproteinase 9MiceMice, Inbred C57BLReverse Transcriptase Polymerase Chain ReactionDNA PrimersFibrinolysinInflammation MediatorsMatrix Metalloproteinase 9

Identifiers

PMID24791857
OpenAlexW2038091965

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.