ArticleJournal of the American Heart Association2017
Transforming Growth Factor-β Receptor III is a Potential Regulator of Ischemia-Induced Cardiomyocyte Apoptosis.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Obstetric and perinatal outcomes in women with cerebrovascular accident vs. transient ischemic attack: an evaluation of a population database.Archives of gynecology and obstetrics · 2024Article
- Transforming growth factor-β in myocardial disease.Nature reviews. Cardiology · 2022Review
- Systematic Bioinformatics Analysis Based on Public and Second-Generation Sequencing Transcriptome Data: A Study on the Diagnostic Value and Potential Mechanisms of Immune-Related Genes in Acute Myocardial Infarction.Frontiers in cardiovascular medicine · 2022Article
- Differential miRNAs in acute spontaneous coronary artery dissection: Pathophysiological insights from a potential biomarker.EBioMedicine · 2021Article
- Endophilin A2-mediated alleviation of endoplasmic reticulum stress-induced cardiac injury involves the suppression of ERO1α/IPInternational journal of biological sciences · 2021Article
- Deciphering the Plasma Proteome of Type 2 Diabetes.Diabetes · 2020Article
- Exosomes: A Potential Therapeutic Tool Targeting Communications between Tumor Cells and Macrophages.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Review
- Knockdown of endogenous RNF4 exacerbates ischaemia-induced cardiomyocyte apoptosis in mice.Journal of cellular and molecular medicine · 2020Article
- LncRNA ACART protects cardiomyocytes from apoptosis by activating PPAR-γ/Bcl-2 pathway.Journal of cellular and molecular medicine · 2020Article
- Deficiency of mouse mast cell protease 4 mitigates cardiac dysfunctions in mice after myocardium infarction.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial infarction (MI) is often accompanied by cardiomyocyte apoptosis, which decreases heart function and leads to an increased risk of heart failure. The aim of this study was to examine the effects of transforming growth factor-β receptor III (TGFβR3) on cardiomyocyte apoptosis during MI. METHODS AND
resultsAn MI mouse model was established by left anterior descending coronary artery ligation. Cell viability, apoptosis, TGFβR3, and mitogen-activated protein kinase signaling were assessed by methylthiazolyldiphenyl-tetrazolium bromide assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, immunofluorescence, electron microscopy, and Western blotting. Our results demonstrated that TGFβR3 expression in the border region of the heart was dynamically changed during MI. After stimulation with H
conclusionsTGFβR3 promotes apoptosis of cardiomyocytes via a p38 pathway-associated mechanism, and loss of TGFβR3 reduces MI injury, which suggests that TGFβR3 may serve as a novel therapeutic target for MI.
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