Evidence map›Paper›PMID 32237065›Full record

ArticleImmunity, inflammation and disease2020

α2AP is associated with the development of lupus nephritis through the regulation of plasmin inhibition and inflammatory responses.

Yosuke Kanno, Mei Miyashita, Mariko Seishima, Osamu Matsuo

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

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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

16 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Yosuke KannoDepartment of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kyoto, Japan.ORCID 0000-0001-9741-2113
Mei MiyashitaDepartment of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kyoto, Japan.
Mariko SeishimaDepartment of Dermatology, Gifu University Graduate School of Medicine, Gifu, Japan.
Osamu MatsuoKindai University Faculty of Medicine, Osakasayama, Japan.
Gifu University · JPDoshisha Women's College of Liberal Arts · JPKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionLupus nephritis (LN) is a common complication of systemic lupus erythematosus (SLE), which is a chronic autoimmune disease. However, the detailed mechanisms underlying this disorder have remained unclear. Alpha2-antiplasmin (α2AP) is known to perform various functions, such as plasmin inhibition and cytokine production, and to be associated with immune and inflammatory responses.

methodsWe investigated the roles of α2AP in the pathogenesis of LN using a pristane-induced lupus mouse model.

resultsThe levels of plasmin-α2AP complex and α2AP were elevated in the lupus model mice. In addition, α2AP deficiency attenuated the pristane-induced glomerular cell proliferation, mesangial matrix expansion, collagen production, fibrin deposition, immunoglobulin G deposition, and proinflammatory cytokine production in the model mice. We also showed that interferon-γ (IFN-γ), which is an essential inducer of LN, induced α2AP production through the c-Jun N-terminal kinase (JNK) pathway in fibroblasts. In addition, plasmin attenuated the IFN-γ-induced proinflammatory cytokine production through the AMPK pathway in macrophages, and α2AP eliminated these effects. Furthermore, we showed that α2AP induced proinflammatory cytokine production through the ERK1/2 and JNK pathways in macrophages.

conclusionα2AP regulates the inflammatory responses through plasmin inhibition and proinflammatory cytokine production and is associated with the development of LN. Our findings may be used to develop a novel therapeutic approach for SLE.

Indexed as

Lupus NephritisAnimalsAntifibrinolytic AgentsCytokinesFibrinolysinFibroblastsMiceAntifibrinolytic AgentsCytokinesFibrinolysinAlpha2-antiplasmininflammationlupus nephritis

Identifiers

PMID32237065
PMCPMC7416015
OpenAlexW3014843006

What OpenQuestion holds

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LicenceCC BY
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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.