Evidence map›Paper›PMID 31723053›Full record

ArticleJCI insight2019

Xanthine oxidase inhibitor ameliorates postischemic renal injury in mice by promoting resynthesis of adenine nucleotides.

Kentaro Fujii, Akiko Kubo, Kazutoshi Miyashita, Masaaki Sato, Aika Hagiwara, Hiroyuki Inoue, Masaki Ryuzaki, Masanori Tamaki, Takako Hishiki, Noriyo Hayakawa and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Preclinical models versus clinical renal ischemia reperfusion injury: A systematic review based on metabolic signatures.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
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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 2 institutions in 1 country.

Kentaro FujiiDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Akiko KuboDepartment of Biochemistry, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Kazutoshi MiyashitaDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Masaaki SatoDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Aika HagiwaraDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Hiroyuki InoueDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Masaki RyuzakiDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Masanori TamakiDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Takako HishikiDepartment of Biochemistry, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Noriyo HayakawaClinical and Translational Research Center, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Yasuaki KabeDepartment of Biochemistry, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Hiroshi ItohDivision of Endocrinology and Metabolism and Nephrology, Department of Internal Medicine and.
Makoto SuematsuDepartment of Biochemistry, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Keio University · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although oxidative stress plays central roles in postischemic renal injury, region-specific alterations in energy and redox metabolism caused by short-duration ischemia remain unknown. Imaging mass spectrometry enabled us to reveal spatial heterogeneity of energy and redox metabolites in the postischemic murine kidney. After 10-minute ischemia and 24-hour reperfusion (10mIR), in the cortex and outer stripes of the outer medulla, ATP substantially decreased, but not in the inner stripes of the outer medulla and inner medulla. 10mIR caused renal injury with elevation of fractional excretion of sodium, although histological damage by oxidative stress was limited. Ischemia-induced NADH elevation in the cortex indicated prolonged production of reactive oxygen species by xanthine oxidase (XOD). However, consumption of reduced glutathione after reperfusion suggested the amelioration of oxidative stress. An XOD inhibitor, febuxostat, which blocks the degradation pathway of adenine nucleotides, promoted ATP recovery and exerted renoprotective effects in the postischemic kidney. Because effects of febuxostat were canceled by silencing of the hypoxanthine phosphoribosyl transferase 1 gene in cultured tubular cells, mechanisms for the renoprotective effects appear to involve the purine salvage pathway, which uses hypoxanthine to resynthesize adenine nucleotides, including ATP. These findings suggest a novel therapeutic approach for acute ischemia/reperfusion renal injury with febuxostat through salvaging high-energy adenine nucleotides.

Indexed as

Acute Kidney InjuryAdenine NucleotidesReperfusion InjuryAnimalsEnzyme InhibitorsFebuxostatKidneyMaleMiceMice, Inbred C57BLOxidative StressReactive Oxygen SpeciesXanthine OxidaseAdenine NucleotidesEnzyme InhibitorsFebuxostatReactive Oxygen SpeciesXanthine OxidaseDrug therapyNephrologyTherapeutics

Identifiers

PMID31723053
PMCPMC6948864
OpenAlexW2987825845

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.