ArticleJournal of molecular and cellular cardiology2021
Suppression of canonical TGF-β signaling enables GATA4 to interact with H3K27me3 demethylase JMJD3 to promote cardiomyogenesis.
Article in Journal of molecular and cellular cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Cardiac Regeneration: New Insights Into the Frontier of Ischemic Heart Failure Therapy.Frontiers in bioengineering and biotechnology · 2020Pooled it
- Advances in fibroblast-based cardiac reprogramming in the treatment of heart disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Direct fibroblast reprogramming: an emerging strategy for treating organic fibrosis.Journal of translational medicine · 2025Review
- Review
- Investigation of Monogenic Diabetes Genes in Thai Children with Autoantibody Negative Diabetes Requiring Insulin.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Amniotic membrane, a novel bioscaffold in cardiac diseases: from mechanism to applications.Frontiers in bioengineering and biotechnology · 2024Review
- The role of pioneer transcription factors in the induction of direct cellular reprogramming.Regenerative therapy · 2023Review
- Cellular reprogramming of fibroblasts in heart regeneration.Journal of molecular and cellular cardiology · 2023Review
- Single-cell multiomics reveals the complexity of TGFβ signalling to chromatin in iPSC-derived kidney organoids.Communications biology · 2022Article
- Fibroblast fate determination during cardiac reprogramming by remodeling of actin filaments.Stem cell reports · 2022Article
- Transforming growth factor-β in myocardial disease.Nature reviews. Cardiology · 2022Review
- Direct reprogramming as a route to cardiac repair.Seminars in cell & developmental biology · 2022Review
- The role of metabolism in directed differentiation versus trans-differentiation of cardiomyocytes.Seminars in cell & developmental biology · 2022Review
- Circulating microRNA: Myocardium-derived prenatal biomarker of ventricular septal defects.Frontiers in genetics · 2022Article
- Manipulating Cardiomyocyte Plasticity for Heart Regeneration.Frontiers in cell and developmental biology · 2022Review
- Control of cardiomyocyte differentiation timing by intercellular signaling pathways.Seminars in cell & developmental biology · 2021Review
- Advanced Technologies to Target Cardiac Cell Fate Plasticity for Heart Regeneration.International journal of molecular sciences · 2021Review
- Inhibition of CREB-CBP Signaling Improves Fibroblast Plasticity for Direct Cardiac Reprogramming.Cells · 2021Article
- Dynamic Patterns of N6-Methyladenosine Profiles of Messenger RNA Correlated with the Cardiomyocyte Regenerability during the Early Heart Development in Mice.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Direct reprogramming of fibroblasts into cardiomyocytes (CMs) represents a promising strategy to regenerate CMs lost after ischemic heart injury. Overexpression of GATA4, HAND2, MEF2C, TBX5, miR-1, and miR-133 (GHMT2m) along with transforming growth factor beta (TGF-β) inhibition efficiently promote reprogramming. However, the mechanisms by which TGF-β blockade promotes cardiac reprogramming remain unknown. Here, we identify interactions between the histone H3 lysine 27 trimethylation (H3K27me3) demethylase JMJD3, the SWI/SNF remodeling complex subunit BRG1, and cardiac transcription factors. Furthermore, canonical TGF-β signaling regulates the interaction between GATA4 and JMJD3. TGF-β activation impairs the ability of GATA4 to bind target genes and prevents demethylation of H3K27 at cardiac gene promoters during cardiac reprogramming. Finally, a mutation in GATA4 (V267M) that is associated with congenital heart disease exhibits reduced binding to JMJD3 and impairs cardiomyogenesis. Thus, we have identified an epigenetic mechanism wherein canonical TGF-β pathway activation impairs cardiac gene programming, in part by interfering with GATA4-JMJD3 interactions.
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Registered trials
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.