Evidence map›Paper›PMID 29636091›Full record

ArticleArthritis research & therapy2018

Dysregulated heme oxygenase-1

Daiga Kishimoto, Yohei Kirino, Maasa Tamura, Mitsuhiro Takeno, Yosuke Kunishita, Kaoru Takase-Minegishi, Hiroto Nakano, Ikuma Kato, Kiyotaka Nagahama, Ryusuke Yoshimi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
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  6. Primary immunodeficiency as a cause of immune-mediated kidney diseases.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  7. Article
  8. Article
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  15. Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2022
    Review
  16. Review
  17. CircRTN4 aggravates mesangial cell dysfunction by activating the miR-513a-5p/FN axis in lupus nephritis.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  18. Review
  19. Article
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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

13 authors at 4 institutions in 1 country.

Daiga KishimotoDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan.
Yohei KirinoDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan. kirino@yokohama-cu.ac.jp.ORCID 0000-0002-9488-661X
Maasa TamuraDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan.
Mitsuhiro TakenoDepartment of Allergy and Rheumatology, Nippon Medical School Graduate School of Medicine, Tokyo, Japan.
Yosuke KunishitaDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan.
Kaoru Takase-MinegishiDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan.
Hiroto NakanoDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan.
Ikuma KatoDepartment of Molecular Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kiyotaka NagahamaDepartment of Pathology, Kyorin University School of Medicine, Tokyo, Japan.
Ryusuke YoshimiDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan.
Kazuhiko IgarashiDepartment of Biochemistry, Tohoku University School of Medicine, Sendai, Japan.
Ichiro AokiDepartment of Molecular Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Hideaki NakajimaDepartment of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-Ku, Yokohama, 236-0004, Japan.
Yokohama City University · JPKyorin University · JPNippon Medical School · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInnate immunity including macrophages (Mϕ) in lupus nephritis (LN) has been gaining attention, but roles of Mϕ in LN remain uncertain.

methodsImmunohistochemical staining was performed to determine CD68, CD163, heme oxygenase (HO)-1 (a stress-inducible heme-degrading enzyme with anti-inflammatory property), pSTAT1, and CMAF-expressing Mϕ in the glomeruli of patients with LN. Effects of type I interferons on the expression levels of CD163, HO-1, BTB and CNC homology 1 (Bach1; a transcriptional HO-1 repressor), interleukin (IL)-6, and IL-10 by human M2-like Mϕ, which were differentiated in vitro from peripheral monocytes with macrophage colony-stimulating factor, were assessed by RT-PCR and immunocytostaining. Clinical manifestations, anti-double-stranded DNA (anti-dsDNA), and local HO-1 expression were compared in Bach1-deficient and wild-type MRL/lpr mice.

resultsThe number of glomerular M2-like Mϕ correlated with the amounts of proteinuria in patients with LN. Unlike monocyte-derived M2-like Mϕ, HO-1 expression was defective in the majority of glomerular M2-like Mϕ of patients with LN. Stimulation of human M2-like Mϕ with type I interferons led to reduced HO-1 expression and increased Bach1 and IL-6 expression. Bach1-deficient MRL/lpr mice exhibited increased HO-1 expression in kidneys, prolonged survival, reduced urine proteins, and serum blood urea nitrogen levels, but serum anti-dsDNA antibody levels were comparable. Increased expression of CD163 and HO-1 was found in peritoneal Mϕ from Bach1-deficient MRL/lpr mice.

conclusionsOur data suggest that dysregulated M2-like Mϕ play a proinflammatory role in LN. Bach1 is a potential therapeutic target that could restore the anti-inflammatory property of M2 Mϕ.

Indexed as

AdultAnimalsBasic-Leucine Zipper Transcription FactorsCells, CulturedFemaleHeme Oxygenase-1HumansInterferon Type ILupus NephritisMacrophagesMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutYoung AdultBach1 protein, mouseBasic-Leucine Zipper Transcription FactorsHeme Oxygenase-1Hmox1 protein, mouseInterferon Type IMembrane ProteinsBach1Heme oxygenase 1Lupus nephritisMacrophage polarizationType I interferons

Identifiers

PMID29636091
PMCPMC5894134
OpenAlexW2805788731

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.