ArticleScientific reports2021
Cardiomyocyte-specific deletion of β-catenin protects mouse hearts from ventricular arrhythmias after myocardial infarction.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Histamine N-methyltransferase upregulation, cardiac hypertrophy, and heart failure.European heart journal · 2026Article
- Targeting Wnt Pathways with Small Molecules as New Approach in Cardiovascular Disease.Current cardiology reviews · 2025Review
- High Glucose Sensitizes Male and Female Rat Cardiomyocytes to Wnt/β-Catenin Signaling.Biomolecules · 2024Article
- The role of miR-128 and MDFI in cardiac hypertrophy and heart failure: Mechanistic.Journal of cellular and molecular medicine · 2024Article
- Proteomic analysis of transcription factors involved in the alteration of ischemic mouse heart as modulated by MSC exosomes.Biochemistry and biophysics reports · 2023Article
- The role of β-catenin in cardiac diseases.Frontiers in pharmacology · 2023Review
- WNT links metabolism and cell cycle in postnatal cardiomyocytes.The journal of cardiovascular aging · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Wnt/β-catenin signaling is activated in the heart after myocardial infarction (MI). This study aims to investigate if β-catenin deletion affects post-MI ion channel gene alterations and ventricular tachycardias (VT). MI was induced by permanent ligation of left anterior descending artery in wild-type (WT) and cardiomyocyte-specific β-catenin knockout (KO) mice. KO mice showed reduced susceptibility to VT (18% vs. 77% in WT) at 8 weeks after MI, associated with reduced scar size and attenuated chamber dilation. qPCR analyses of both myocardial tissues and purified cardiomyocytes demonstrated upregulation of Wnt pathway genes in border and infarct regions after MI, including Wnt ligands (such as Wnt4) and receptors (such as Fzd1 and Fzd2). At 1 week after MI, cardiac sodium channel gene (Scn5a) transcript was reduced in WT but not in KO hearts, consistent with previous studies showing Scn5a inhibition by Wnt/β-catenin signaling. At 8 weeks after MI when Wnt genes have declined, Scn5a returned to near sham levels and K
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