Evidence map›Paper›PMID 33448693›Full record

ArticleFEBS open bio2021

Tissue xanthine oxidoreductase activity in a mouse model of aristolochic acid nephropathy.

Takeo Ishii, Tomohiro Kumagae, Hiromichi Wakui, Shingo Urate, Shohei Tanaka, Eriko Abe, Toru Suzuki, Takahiro Yamaji, Sho Kinguchi, Ryu Kobayashi and 4 more

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

14 authors at 4 institutions in 1 country.

Takeo IshiiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.ORCID 0000-0002-5960-260X
Tomohiro KumagaeDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Hiromichi WakuiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Shingo UrateDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Shohei TanakaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Eriko AbeDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Toru SuzukiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Takahiro YamajiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Sho KinguchiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Ryu KobayashiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Kotaro HaruharaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Takashi NakamuraMedical Affairs Department, Sanwa Kagaku Kenkusho., Co., Ltd, Aichi, Japan.ORCID 0000-0003-2324-3569
Shuzo KobayashiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Kouichi TamuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Yokohama City University · JPShonan Kamakura General Hospital · JPDaiyukai General Hospital · JPRiso Kagaku (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Xanthine oxidoreductase (XOR) is a critical enzyme in purine metabolism and uric acid production, and its levels are reported to increase during stress, thereby promoting organ damage. Herein, we investigated the activity of XOR in a mouse model of aristolochic acid I (AA)-induced nephropathy, a type of nephrotoxic chronic kidney disease (CKD). A persistent decrease in renal function was observed in mice up to 4 weeks after 4 weeks of AA (2.5 mg kg

Indexed as

AnimalsAristolochic AcidsDisease Models, AnimalFibrosisHumansKidney TubulesMaleMiceRenal Insufficiency, ChronicXanthine Dehydrogenasearistolochic acid IAristolochic AcidsXanthine Dehydrogenasearistolochic acidmouse modelnephropathyxanthine oxidoreductase

Identifiers

PMID33448693
PMCPMC7876505
OpenAlexW3119957406

What Socratic holds

Textmetadata
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 Socratic graph.