Evidence map›Paper›PMID 39863758›Full record

ArticleScientific reports2025

Pseudogenization of the Slc23a4 gene is necessary for the survival of Xdh-deficient mice.

Kazuki Terada, Tamaki Watanabe, Nobuhiro Yasuno, Toshio Ohtsubo, Shigeru Shibata, Kimiyoshi Ichida, Makoto Hosoyamada

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Mechanism investigation ofOpen life sciences · 2026
    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

7 authors.

Kazuki TeradaLaboratory of Human Physiology and Pathology, Faculty of Pharmaceutical Sciences, Teikyo University, Tokyo, Japan.
Tamaki WatanabeLaboratory of Hospital Pharmacy, Faculty of Pharmaceutical Sciences, Teikyo University, Tokyo, Japan.
Nobuhiro YasunoLaboratory of Hospital Pharmacy, Faculty of Pharmaceutical Sciences, Teikyo University, Tokyo, Japan.
Toshio OhtsuboJapanese Red Cross Fukuoka Hospital, Fukuoka, Japan.
Shigeru ShibataDivision of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.
Kimiyoshi IchidaChiba Health Promotion Center, East Japan Railway Company, Chiba, Japan.
Makoto HosoyamadaLaboratory of Human Physiology and Pathology, Faculty of Pharmaceutical Sciences, Teikyo University, Tokyo, Japan. hosoyamd@pharm.teikyo-u.ac.jp.

Funding

Grants-in Aid for Scientific Research from Japan Society for the Promotion of Science No. 26460347, No. 17K08605 and No. 22K08320
6 · The paper itself

Abstract

In most patients with type 1 xanthinuria caused by mutations in the xanthine dehydrogenase gene (XDH), no clinical complications, except for urinary stones, are observed. In contrast, all Xdh(- / -) mice die due to renal failure before reaching adulthood at 8 weeks of age. Hypoxanthine or xanthine levels become excessive and thus toxic in Xdh(- / -) mice because enhancing the activity of hypoxanthine phosphoribosyl transferase (HPRT), which is an enzyme that uses hypoxanthine as a substrate, slightly increases the life span of these mice. In this study, we targeted the mouse intestinal sodium-dependent nucleobase transporter (SNBT) gene (Slc23a4), which is a pseudogene in humans. Hprt(high)Xdh(- / -)Slc23a4(- / -) mice had a longer life span and reached adulthood. The urinary xanthine excretion of these mice was 20-fold greater than that of patients with type 1 xanthinuria. The urinary hypoxanthine/xanthine ratio of Hprt(high)Xdh(- / -)Slc23a4(- / -) mice was lower than that of patients with type 1 xanthinuria. Hprt(high)Xdh(- / -)Slc23a4(- / -) mice exhibited renal impairment, accompanied by high plasma creatinine levels and anemia. Moreover, female Hprt(high)Xdh(- / -)Slc23a4(- / -) mice produced offspring that did not survive. In conclusion, for the first time, we established that Xdh(- / -) mice survive to adulthood.

Indexed as

Nucleobase Transport ProteinsPseudogenesXanthine DehydrogenaseAnimalsFemaleHumansHypoxanthineHypoxanthine PhosphoribosyltransferaseLongevityMaleMiceMice, KnockoutXanthineHypoxanthineHypoxanthine PhosphoribosyltransferaseNucleobase Transport ProteinsXanthineXanthine DehydrogenaseHypoxanthineSodium dependent nucleobase transporterType 1 xanthinuriaXanthineXanthine dehydrogenase

Identifiers

PMID39863758
PMCPMC11762782

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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.