ArticleInternational journal of molecular sciences2021
Excess TGF-β1 Drives Cardiac Mesenchymal Stromal Cells to a Pro-Fibrotic Commitment in Arrhythmogenic Cardiomyopathy.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Desmoplakin Mutations in Cardiac Fibroblasts Cause TGFβ1-Mediated Pathological Fibrogenesis in Desmoplakin Cardiomyopathy Via Beclin-1 Regulation.Circulation research · 2026Article
- Epigenetic Drugs Splitomicin, Suberohydroxamic Acid, CPTH6, BVT-948, and PBIT Moderate Fibro-Fatty Development in Arrhythmogenic Cardiomyopathy.Biomolecules · 2025Article
- Arrhythmogenic Cardiomyopathy and Biomarkers: A Promising Perspective?Journal of clinical medicine · 2025Review
- Analysis of effector/memory regulatory T cells from arrhythmogenic cardiomyopathy patients identified IL-32 as a novel player in ACM pathogenesis.Cell death & disease · 2025Article
- Cardiomyocyte and stromal cell cross-talk influences the pathogenesis of arrhythmogenic cardiomyopathy: a multi-level analysis uncovers DLK1-NOTCH pathway role in fibro-adipose remodelling.Cell death discovery · 2024Article
- Hypertrophic cardiomyopathy-associated mutations drive stromal activation via EGFR-mediated paracrine signaling.Science advances · 2024Article
- In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models.Cells · 2024Review
- TGF-β1-triggered BMI1 and SMAD2 cooperatively regulate miR-191 to modulate bone formation.Molecular therapy. Nucleic acids · 2024Article
- Recent Advances of MSCs in Renal IRI: From Injury to Renal Fibrosis.Bioengineering (Basel, Switzerland) · 2024Review
- Patient-specific primary and pluripotent stem cell-derived stromal cells recapitulate key aspects of arrhythmogenic cardiomyopathy.Scientific reports · 2023Article
- Store-Operated CaJournal of clinical medicine · 2023Review
- Omics Analyses of Stromal Cells from ACM Patients Reveal Alterations in Chromatin Organization and Mitochondrial Homeostasis.International journal of molecular sciences · 2023Article
- CaJournal of translational medicine · 2022Article
- GCN5 contributes to intracellular lipid accumulation in human primary cardiac stromal cells from patients affected by Arrhythmogenic cardiomyopathy.Journal of cellular and molecular medicine · 2022Article
- Purinergic Receptor P2Y2 Stimulation Averts Aortic Valve Interstitial Cell Calcification and Myofibroblastic Activation.Biomedicines · 2022Article
- Toward Human Models of Cardiorenal SyndromeFrontiers in cardiovascular medicine · 2022Review
- Nicotinic Acid Adenine Dinucleotide Phosphate Induces Intracellular CaFrontiers in cell and developmental biology · 2022Article
- Insights Into Genetics and Pathophysiology of Arrhythmogenic Cardiomyopathy.Current heart failure reports · 2021Review
- Inflammation and Immune Response in Arrhythmogenic Cardiomyopathy: State-of-the-Art Review.Circulation · 2021Article
- Compromised Biomechanical Properties, Cell-Cell Adhesion and Nanotubes Communication in Cardiac Fibroblasts Carrying the Lamin A/C D192G Mutation.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Arrhythmogenic Cardiomyopathy (ACM) is characterized by the replacement of the myocardium with fibrotic or fibro-fatty tissue and inflammatory infiltrates in the heart. To date, while ACM adipogenesis is a well-investigated differentiation program, ACM-related fibrosis remains a scientific gap of knowledge. In this study, we analyze the fibrotic process occurring during ACM pathogenesis focusing on the role of cardiac mesenchymal stromal cells (C-MSC) as a source of myofibroblasts. We performed the ex vivo studies on plasma and right ventricular endomyocardial bioptic samples collected from ACM patients and healthy control donors (HC). In vitro studies were performed on C-MSC isolated from endomyocardial biopsies of both groups. Our results revealed that circulating TGF-β1 levels are significantly higher in the ACM cohort than in HC. Accordingly, fibrotic markers are increased in ACM patient-derived cardiac biopsies compared to HC ones. This difference is not evident in isolated C-MSC. Nevertheless, ACM C-MSC are more responsive than HC ones to TGF-β1 treatment, in terms of pro-fibrotic differentiation and higher activation of the SMAD2/3 signaling pathway. These results provide the novel evidence that C-MSC are a source of myofibroblasts and participate in ACM fibrotic remodeling, being highly responsive to ACM-characteristic excess TGF-β1.
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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.