Evidence map›Paper›PMID 37558983›Full record

ArticleThe journal of physiological sciences : JPS2023

Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice.

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

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The journal of physiological sciences : JPS, 2023. 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
0.2field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Review
  2. 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 1 institution in 1 country.

Michinori Tsunoda *Department of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Ichiro Matsuo *Department of Periodontology, 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.
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.
Aiko ItoDepartment of Orthodontology, Tsurumi University School of Dental Medicine, 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.
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.
Kazuhiro GomiDepartment of Periodontology, 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.ORCID 0000-0001-8747-7941
Tsurumi University · JP

Funding

Japan Society for the Promotion of Science 19K24109Japan 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

In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/Ca

Indexed as

CardiomyopathiesVidarabineAnimalsHeartLipopolysaccharidesMicePorphyromonas gingivalisLipopolysaccharidesVidarabineAdenylyl cyclaseApoptosisFibrosisHeart failurePeriodontitisSignal transductionβ-Adrenergic signaling

Identifiers

PMID37558983
PMCPMC10717078
OpenAlexW4385707527

What OpenQuestion 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 OpenQuestion graph.