Evidence map›Paper›PMID 30544662›Full record

ArticleInternational journal of molecular sciences2018

The Xanthine Oxidase Inhibitor Febuxostat Suppresses the Progression of IgA Nephropathy, Possibly via Its Anti-Inflammatory and Anti-Fibrotic Effects in the gddY Mouse Model.

Masa-Ki Inoue, Takeshi Yamamotoya, Yusuke Nakatsu, Koji Ueda, Yuki Inoue, Yasuka Matsunaga, Hideyuki Sakoda, Midori Fujishiro, Hiraku Ono, Kenichi Morii and 5 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.9field-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

6 citing papers in PubMed, 19 citations in OpenAlex.

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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

15 authors at 8 institutions in 2 countries.

Masa-Ki InoueDepartment of Medical Science, Graduate School of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. b131831@hiroshima-u.ac.jp.
Takeshi YamamotoyaDepartment of Medical Science, Graduate School of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. ymmty@hiroshima-u.ac.jp.
Yusuke NakatsuDepartment of Medical Science, Graduate School of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. nakatsu@hiroshima-u.ac.jp.
Koji UedaDepartment of Medical Science, Graduate School of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. urouedakouji@yahoo.co.jp.
Yuki InoueDepartment of Medical Science, Graduate School of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. iyuki_ym@yahoo.co.jp.
Yasuka MatsunagaCenter for Translational Research in Infection & Inflammation, School of Medicine, Tulane University, 6823 St. Charles Avenue, New Orleans, LA 70118, USA. ymatsunaga@tulane.edu.
Hideyuki SakodaDivision of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan. hideyuki_sakoda@med.miyazaki-u.ac.jp.
Midori FujishiroDivision of Diabetes and Metabolic Diseases, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan. fujishiro.midori@nihon-u.ac.jp.
Hiraku OnoDepartment of Clinical Cell Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba City, Chiba 260-8670, Japan. hono@chiba-u.jp.
Kenichi MoriiDepartment of Nephrology, Hiroshima University Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. kenichi_morii@yahoo.co.jp.
Kensuke SasakiDepartment of Nephrology, Hiroshima University Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. sasakikuma@gmail.com.
Takao MasakiDepartment of Nephrology, Hiroshima University Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. masakit@hiroshima-u.ac.jp.
Yusuke SuzukiDivision of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan. yusuke@juntendo.ac.jp.
Tomoichiro AsanoDepartment of Medical Science, Graduate School of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima 734-8551, Japan. tasano@hiroshima-u.ac.jp.
Akifumi KushiyamaDivision of Diabetes and Metabolism, The Institute for Adult Diseases, Asahi Life Foundation, Chuo-ku, Tokyo 103-0002, Japan. a-kushiyama@asahi-life.or.jp.ORCID 0000-0003-1385-7487
Hiroshima University · JPHiroshima University Hospital · JPChiba University · JPJuntendo University · JPNihon University · JPThe Institute of Medical Science, Asahi Life Foundation · JPTulane University · USUniversity of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent clinical studies have demonstrated the protective effect of xanthine oxidase (XO) inhibitors against chronic kidney diseases, although the underlying molecular mechanisms remain unclear. However, to date, neither clinical nor basic research has been carried out to elucidate the efficacy of XO inhibitor administration for IgA nephropathy. We thus investigated whether febuxostat, an XO inhibitor, exerts a protective effect against the development of IgA nephropathy, using gddY mice as an IgA nephropathy rodent model. Eight-week-old gddY mice were provided drinking water with (15 μg/mL) or without febuxostat for nine weeks and then subjected to experimentation. Elevated serum creatinine and degrees of glomerular sclerosis and fibrosis, judged by microscopic observations, were significantly milder in the febuxostat-treated than in the untreated gddY mice, while body weights and serum IgA concentrations did not differ between the two groups. In addition, elevated mRNA levels of inflammatory cytokines such as TNFα, MCP-1, IL-1β, and IL-6, collagen isoforms and chemokines in the gddY mouse kidneys were clearly normalized by the administration of febuxostat. These data suggest a protective effect of XO inhibitors against the development of IgA nephropathy, possibly via suppression of inflammation and its resultant fibrotic changes, without affecting the serum IgA concentration.

Indexed as

Disease ProgressionAnimalsAnti-Inflammatory AgentsChemokinesEndoplasmic Reticulum StressFebuxostatFemaleFibrosisGene Expression RegulationGlomerulonephritis, IGAInflammation MediatorsKidneyMice, Inbred BALB CXanthine OxidaseAnti-Inflammatory AgentsChemokinesFebuxostatInflammation MediatorsXanthine OxidaseFebuxostatFibrosisIgA nephropathyInflammationxanthine oxidase inhibitor

Identifiers

PMID30544662
PMCPMC6320819
OpenAlexW2903788790

What OpenQuestion holds

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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.