Evidence map›Paper›PMID 35392757›Full record

ArticleRenal failure2022

Glomerular endothelial expression of type I IFN-stimulated gene, DExD/H-Box helicase 60 via toll-like receptor 3 signaling: possible involvement in the pathogenesis of lupus nephritis.

Takao Karasawa, Riko Sato, Tadaatsu Imaizumi, Shun Hashimoto, Masashi Fujita, Tomomi Aizawa, Koji Tsugawa, Shogo Kawaguchi, Kazuhiko Seya, Kiminori Terui and 1 more

Open access · goldAbstract read
In one paragraph

Article in Renal failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-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

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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. The Impact of Genetic Factors in Ménière's Disease.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Type I IFN in Glomerular Disease: Scarring beyond the STING.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
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

11 authors at 2 institutions in 1 country.

Takao KarasawaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Riko SatoDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Tadaatsu ImaizumiDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Shun HashimotoDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Masashi FujitaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Tomomi AizawaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Koji TsugawaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Shogo KawaguchiDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Kazuhiko SeyaDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Kiminori TeruiDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Hiroshi TanakaDepartment of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan.
Hirosaki University Hospital · JPHirosaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSustained type I interferon (IFN) activation

methodsWe treated cultured human glomerular endothelial cells (GECs) with polyinosinic-polycytidylic acid (poly IC), R848, and CpG (TLR3, TLR7, and TLR9 agonists, respectively) and analyzed the expression of DExD/H-Box Helicase 60 (DDX60), a representative ISG, using quantitative reverse transcription-polymerase chain reaction and western blotting. Additionally, RNA interference against IFN-β or DDX60 was performed. Furthermore, cleavage of caspase 9 and poly (ADP-ribose) polymerase (PARP), markers of cells undergoing apoptosis, was examined using western blotting. We conducted an immunofluorescence study to examine endothelial DDX60 expression in biopsy specimens from patients with LN.

resultsWe observed that endothelial expression of DDX60 was induced by poly IC but not by R848 or CpG, and RNA interference against IFN-β inhibited poly IC-induced DDX60 expression. DDX60 knockdown induced cleavage of caspase 9 and PARP. Intense endothelial DDX60 expression was observed in biopsy specimens from patients with diffuse proliferative LN.

conclusionGlomerular endothelial DDX60 expression may prevent apoptosis, which is involved in the pathogenesis of LN. Modulating the upregulation of the regional innate immune system

Indexed as

DEAD-box RNA HelicasesLupus NephritisToll-Like Receptor 3Antiviral AgentsCaspase 9Endothelial CellsHumansInterferon-betaPoly(ADP-ribose) Polymerase InhibitorsPoly I-CAntiviral AgentsCaspase 9DDX60 protein, humanDEAD-box RNA HelicasesInterferon-betaPoly(ADP-ribose) Polymerase InhibitorsPoly I-CTLR3 protein, humanToll-Like Receptor 3DExD/H-Box Helicase 60 (DDX60)Glomerular endothelial cellslupus nephritisPoly (ADP-ribose) polymerase (PARP)toll-like receptor

Identifiers

PMID35392757
PMCPMC9004514
OpenAlexW4223598256

What OpenQuestion holds

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LicenceCC BY-NC
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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.