Evidence map›Paper›PMID 37968296›Full record

ArticleScientific reports2023

Effects of the angiotensin-converting enzyme inhibitor captopril on occlusal-disharmony-induced cardiac dysfunction in mice.

Aiko Ito, Yoshiki Ohnuki, Kenji Suita, Ichiro Matsuo, Misao Ishikawa, Takao Mitsubayashi, Yasumasa Mototani, Kenichi Kiyomoto, Michinori Tsunoda, Akinaka Morii and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 4 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

14 authors at 1 institution in 1 country.

Aiko ItoDepartment of Orthodontics, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Yoshiki OhnukiDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Kenji SuitaDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Ichiro MatsuoDepartment of Periodontology, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Misao IshikawaDepartment of Oral Anatomy, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Takao MitsubayashiDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Yasumasa MototaniDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Kenichi KiyomotoDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Michinori TsunodaDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Akinaka MoriiDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Megumi NariyamaDepartment 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.
Hiroshi TomonariDepartment of Orthodontics, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Satoshi OkumuraDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan. okumura-s@tsurumi-u.ac.jp.
Tsurumi University · JP

Funding

Japan Society for the Promotion of Science 20K10304Japan Society for the Promotion of Science 20K10305Japan Society for the Promotion of Science 21K10242Japan Society for the Promotion of Science 21K17171Japan Society for the Promotion of Science 22K10255Japan Society for the Promotion of Science 22K21003
6 · The paper itself

Abstract

Occlusal disharmony is known to affect not only the oral cavity environment, but also the autonomic nervous system in the heart. Since the renin-angiotensin system (RAS) inhibitor captopril (Cap) is one of the first-line drugs for preventing cardiac remodeling in patients with heart failure, we hypothesized that Cap might prevent cardiac dysfunction induced by occlusal disharmony. Here, to test this idea, we used our bite-opening (BO) mouse model, which was developed by cementing a suitable appliance onto the mandibular incisor. Mice were divided into four groups: (1) Control, (2) BO, (3) Cap, and (4) BO + Cap. After 2 weeks, we evaluated cardiac function by echocardiography and confirmed that cardiac function was significantly decreased in the BO group compared to the control, while Cap ameliorated the dysfunction. Cardiac fibrosis, myocyte apoptosis and oxidative stress-induced myocardial damage in the BO group were significantly increased versus the control, and these increases were suppressed by Cap. Cardiac dysfunction induced by BO was associated with dual phosphorylation on PKCδ (Tyr-311/Thr-505), leading to activation of CaMKII with increased phosphorylation of RyR2 and phospholamban. Our results suggest that the RAS might play an important role in the development of cardiac diseases induced by occlusal anomalies.

Indexed as

Angiotensin-Converting Enzyme InhibitorsHeart FailureAnimalsCaptoprilEnzyme InhibitorsHeartHumansMiceMyocardiumAngiotensin-Converting Enzyme InhibitorsCaptoprilEnzyme Inhibitors

Identifiers

PMID37968296
PMCPMC10651878
OpenAlexW4388696034

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.