Evidence map›Paper›PMID 41764204›Full record

ArticleCell death discovery2026

BACH2 links β1-adrenergic receptor/β-arrestin1 signaling to MIAT to inhibit cardiac fibroblast activation and cardiomyocyte apoptosis.

Bruno Moukette, Jian-Peng Teoh, Waleed J Hashmi, Satoshi Kawaguchi, Tatsuya Aonuma, Hamedane Moustapha, Steven S Welc, Simon J Conway, Suthat Liangpunsakul, Lei Yang and 2 more

Abstract read
In one paragraph

Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Bruno MouketteDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Jian-Peng TeohDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Waleed J HashmiDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Satoshi KawaguchiDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Tatsuya AonumaDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Hamedane MoustaphaDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Steven S WelcDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Simon J ConwayHerman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.
Suthat LiangpunsakulDivision of Gastroenterology and Hepatology, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID http://orcid.org/0000-0002-6504-8123
Lei YangHerman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID http://orcid.org/0000-0002-1479-2374
Ankit A DesaiKrannert Cardiovascular Research Center, Indiana University School of Medicine, Indianapolis, IN, USA.
Il-Man KimDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA. ilkim@iu.edu.ORCID http://orcid.org/0000-0002-9268-8337

Funding

Transcriptional Factor SOX2, LncRNA HBL1, microRNA1 and PRC2 Epigenetic Complex Compose a Network to Orchestrate Cardiac Differentiation from Human Pluripotent Stem CellsR01HL147871 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI YANG, LEI · 2019 to 2023
$2.5M
Deciphering a Novel LncRNA-mediated Lipid Droplet Transport System in Human HeartR01HL160856 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI YANG, LEI · 2022 to 2025
$2.2M
Deciphering the novel regulatory mechanisms of neovascularization, cardiomyocyte survival, and endothelial cell-cardiomyocyte crosstalk in myocardial infarctionR01HL180692 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI Il-man Kim · 2025 to 2026
$1.3M
NHLBI NIH HHS R01 HL147871NHLBI NIH HHS R01 HL160856NHLBI NIH HHS R01 HL180692U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01HL180692
6 · The paper itself

Abstract

The myocardial infarction-associated transcript (MIAT), a conserved long noncoding RNA, is upregulated in failing human and murine hearts. We previously demonstrated that systemic or cardiomyocyte (CM)-restricted ablation of MIAT in mice attenuated maladaptive cardiac remodeling following myocardial infarction by suppressing the expression of proapoptotic and profibrotic genes. Despite growing evidence from human and rodent studies implicating MIAT in heart failure, the upstream regulatory pathways controlling its expression remain poorly defined. We hypothesized that MIAT is regulated either by β-arrestin1-mediated β

Identifiers

PMID41764204
PMCPMC13039337

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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.