Evidence map›Paper›PMID 25821355›Full record

ReviewMediators of inflammation2015

Pathogenic roles of macrophage migration inhibitory factor during dengue virus infection.

Yung-Chun Chuang, Hong-Ru Chen, Trai-Ming Yeh

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

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  10. Expression of macrophage migration inhibitory factor inInternational journal of ophthalmology · 2019
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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

3 authors at 1 institution in 1 country.

Yung-Chun ChuangDepartment of Medical Laboratory Science and Biotechnology, Medical College, National Cheng Kung University, Tainan 70101, Taiwan ; Center of Infectious Disease and Signaling Research, Medical College, National Cheng Kung University, Tainan 70101, Taiwan.
Hong-Ru ChenCenter of Infectious Disease and Signaling Research, Medical College, National Cheng Kung University, Tainan 70101, Taiwan ; The Institute of Basic Medical Sciences, Medical College, National Cheng Kung University, Tainan 70101, Taiwan.
Trai-Ming YehDepartment of Medical Laboratory Science and Biotechnology, Medical College, National Cheng Kung University, Tainan 70101, Taiwan ; Center of Infectious Disease and Signaling Research, Medical College, National Cheng Kung University, Tainan 70101, Taiwan ; The Institute of Basic Medical Sciences, Medical College, National Cheng Kung University, Tainan 70101, Taiwan.ORCID 0000-0003-3172-7432
National Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dengue virus (DENV) infection is the most common cause of viral hemorrhagic fever, which can lead to life-threatening dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Hemorrhage and plasma leakage are two major hallmarks of DHF/DSS. Because the mechanisms causing these pathogenic changes are unclear, there is no effective therapy against DHF/DSS. In this review, we focus on the possible pathogenic effects of a pleiotropic cytokine, macrophage migration inhibitory factor (MIF), on the pathogenesis of DENV infection. MIF is a critical mediator of the host immune response and inflammation, and there is a correlation between the serum levels of MIF and disease severity in dengue patients. Furthermore, MIF knock-out mice exhibit less severe clinical disease and lethality. However, the role of MIF in the pathogenesis of DHF/DSS is not limited to immune cell recruitment. Recent evidence indicates that DENV infection induced MIF production and may contribute to vascular hyperpermeability and viral replication during DENV infection. The expression of both adhesion and coagulation molecules on MIF-stimulated monocytes and endothelial cells is also increased, which may contribute to inflammatory and anticoagulatory states during DHF/DSS. Therefore, blocking MIF production or its function may provide a solution for the treatment and prevention of DHF/DSS.

Indexed as

AnimalsCapillary PermeabilityDengueDengue VirusHumansInflammationIntercellular Adhesion Molecule-1Intramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMiceVirus ReplicationIntercellular Adhesion Molecule-1Intramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMIF protein, human

Identifiers

PMID25821355
PMCPMC4363636
OpenAlexW2060135129

What OpenQuestion holds

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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.