Evidence map›Paper›PMID 39837857›Full record

ArticleScientific reports2025

Hypermethylation of Hif3a and Ifltd1 is associated with atrial remodeling in pressure-overload murine model.

Keiko Abe, Tetsuo Sasano, Yurie Soejima, Haruhisa Fukayama, Shigeru Maeda, Tetsushi Furukawa

Abstract read
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. Review
  2. 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

6 authors.

Keiko AbeDepartment of Dental Anesthesiology and Orofacial Pain Management, Institute of Science Tokyo, Tokyo, Japan.
Tetsuo SasanoDepartment of Cardiovascular Medicine, Institute of Science Tokyo, 1-5-45, Yushima, Bunkyo-ku, Tokyo, Japan. sasano.cvm@tmd.ac.jp.
Yurie SoejimaDepartment of Pathology and Anatomical Sciences, Institute of Science Tokyo, Tokyo, Japan.
Haruhisa FukayamaDepartment of Dental Anesthesiology and Orofacial Pain Management, Institute of Science Tokyo, Tokyo, Japan.
Shigeru MaedaDepartment of Dental Anesthesiology and Orofacial Pain Management, Institute of Science Tokyo, Tokyo, Japan.
Tetsushi FurukawaInstitute of Science Tokyo, Tokyo, Japan.

Funding

the Grant-in-Aid for Scientific Research 19K08536the Joint Usage/Research Program of Medical Research Institute, Tokyo Medical and Dental University 16K09494
6 · The paper itself

Abstract

Atrial remodeling is a major pathophysiological mechanism of atrial fibrillation (AF). Atrial remodeling progresses with aging and background diseases, including hypertension, heart failure, and AF itself. However, its mechanism of action and reversibility have not been completely elucidated. In this study, we investigated the involvement of DNA methylation in atrial remodeling. Mice underwent transverse aortic constriction (TAC) to generate a pressure overload model. After 14 days, the TAC-operated mice showed a significant increase in the atrium/body weight ratio and deposition of collagen fibers in the atria. A comprehensive analysis using RNA-sequencing (RNA-Seq) and methyl-CpG-binding domain sequencing (MBD-Seq) in the left atrial tissue identified Hif3a and Ifltd1 as showing increased DNA methylation in their promoter regions and decreased RNA expression. In addition, we created a transient pressure overload model by removing the aortic constriction 3 or 7 days after the initial TAC procedure (R3 or R7 groups). A reduction in RNA expression was achieved at R3 for Hif3a and at R7 for Ifltd1. Heterozygous Dnmt1 gene-targeting mice (Dnmt1

Indexed as

Atrial FibrillationAtrial RemodelingDNA MethylationAnimalsDisease Models, AnimalHeart AtriaMaleMiceMice, Inbred C57BLPromoter Regions, GeneticAtrial fibrillationAtrial remodelingHif3aIfltd1MethylationReverse remodeling

Identifiers

PMID39837857
PMCPMC11751168

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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.