Evidence map›Paper›PMID 40617095›Full record

ArticleThe journal of physiological sciences : JPS2025

Xanthine oxidase inhibitor allopurinol preserves cardiac function after experimental malocclusion induced by occlusal disharmony in mice.

Takao Mitsubayashi, Kenji Suita, Yoshiki Ohnuki, Misao Ishikawa, Aiko Ito, Ichiro Matsuo, Go Miyamoto, Mariko Abe, Akinaka Morii, Yasumasa Mototani and 4 more

Abstract read
In one paragraph

Article in The journal of physiological sciences : JPS, 2025. 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
–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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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.

Takao MitsubayashiDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Kenji SuitaDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Yoshiki OhnukiDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Misao IshikawaDepartment of Anatomy, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Aiko ItoDepartment of Orthodontology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Ichiro MatsuoDepartment of Oral and Maxillofacial Surgery, Ibaraki Medical Center Tokyo Medical University, Ibaraki 300-0395, Japan.
Go MiyamotoDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan; Department of Orthodontology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Mariko AbeDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan; Department of Orthodontology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Akinaka MoriiDepartment of Periodontology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Yasumasa MototaniDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Megumi NariyamaDepartment of Pediatric Dentistry, Tsurumi University School of Dental Medicine, Yokohama 236-8501, Japan.
Ren MatsubaraDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan; Department of Pediatric Dentistry, Tsurumi University School of Dental Medicine, Yokohama 236-8501, Japan.
Yoshio HayakawaDepartment of Dental Anesthesiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan.
Satoshi OkumuraDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama 230-8501, Japan. Electronic address: okumura-s@tsurumi-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress caused by poor oral condition is associated with systemic diseases, including cardiovascular disease. In this work, therefore, we examined the effect of allopurinol, an inhibitor of the reactive oxygen species (ROS)-producing enzyme xanthine oxidase, on cardiac dysfunction in our bite-opening (BO) mouse model, in which a suitable appliance is cemented onto the mandibular incisior. After two weeks, we confirmed that cardiac function was significantly decreased in the BO group compared to the control, while allopurinol ameliorated the dysfunction. The impairment of cardiac function in BO mice was associated with increased production of ROS by xanthine oxidase, leading to the activation of calmodulin kinase II, and altered phosphorylation of ryanodine receptor 2 and phospholamban. These changes were also suppressed by allopurinol. Our results suggest that oxidative stress might play an important role in the development of cardiac dysfunction, and further indicate that allopurinol is protective against BO-induced cardiac dysfunction.

Indexed as

AllopurinolEnzyme InhibitorsHeartMalocclusionXanthine OxidaseAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Disease Models, AnimalMaleMiceOxidative StressReactive Oxygen SpeciesAllopurinolCalcium-Calmodulin-Dependent Protein Kinase Type 2Enzyme InhibitorsReactive Oxygen SpeciesXanthine OxidaseApoptosisFibrosisHeart failureOcclusal disharmonySignal transductionXanthine oxidase

Identifiers

PMID40617095
PMCPMC12271071

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.