ArticleCell stem cell2016
Bmi1 Is a Key Epigenetic Barrier to Direct Cardiac Reprogramming.
Article in Cell stem cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 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
148 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.
- Cardiac Regeneration: New Insights Into the Frontier of Ischemic Heart Failure Therapy.Frontiers in bioengineering and biotechnology · 2020Pooled it
- Integrating delivery systems and microenvironmental cues to accelerate clinical translation of cardiac reprogramming.Materials today. Bio · 2026Review
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- Enhancing cardiomyocyte reprogramming efficiency by targeting cellular senescence is mediated via Rb1 gene.Stem cell research & therapy · 2025Article
- Bmi1 controls auditory sensory epithelial cell proliferation through genome-wide H3K27me3 modifications.Epigenetics & chromatin · 2025Article
- Blocking nuclear receptor Nr4a3 unlocks the senescence barrier to promote direct cardiac reprogramming.Science advances · 2025Article
- In Vivo Targeted Reprogramming of Cardiac Fibroblasts for Heart Regeneration: Advances and Therapeutic Potential.Bioengineering (Basel, Switzerland) · 2025Review
- 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
- Reprogramming of human urine cells into cardiomyocytes via a small molecule cocktail in xeno-free conditions.Communications medicine · 2025Article
- Competing dynamic gene regulatory networks involved in fibroblast reprogramming to hematopoietic progenitor cells.Stem cell reports · 2025Article
- Enhanced fatty acid oxidation via SCD1 downregulation fuels cardiac reprogramming.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Cell reprogramming: methods, mechanisms and applications.Cell regeneration (London, England) · 2025Review
- Cell Reprogramming, Transdifferentiation, and Dedifferentiation Approaches for Heart Repair.International journal of molecular sciences · 2025Review
- Decoding the epigenetic and transcriptional basis of direct cardiac reprogramming.Stem cells (Dayton, Ohio) · 2025Review
- Macrophages suppress cardiac reprogramming of fibroblasts in vivo via IFN-mediated intercellular self-stimulating circuit.Protein & cell · 2024Article
- Control of cell fate upon transcription factor-driven cardiac reprogramming.Current opinion in genetics & development · 2024Review
- Clinical trials in-a-dish for cardiovascular medicine.European heart journal · 2024Review
- Direct Cardiac Reprogramming in the Age of Computational Biology.Journal of cardiovascular development and disease · 2024Review
- Temporal genomics in Hawaiian crickets reveals compensatory intragenomic coadaptation during adaptive evolution.Nature communications · 2024Article
- Modifying miRs for effective reprogramming of fibroblasts to cardiomyocytes.Molecular therapy. Nucleic acids · 2024Article
88 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Direct reprogramming of induced cardiomyocytes (iCMs) suffers from low efficiency and requires extensive epigenetic repatterning, although the underlying mechanisms are largely unknown. To address these issues, we screened for epigenetic regulators of iCM reprogramming and found that reducing levels of the polycomb complex gene Bmi1 significantly enhanced induction of beating iCMs from neonatal and adult mouse fibroblasts. The inhibitory role of Bmi1 in iCM reprogramming is mediated through direct interactions with regulatory regions of cardiogenic genes, rather than regulation of cell proliferation. Reduced Bmi1 expression corresponded with increased levels of the active histone mark H3K4me3 and reduced levels of repressive H2AK119ub at cardiogenic loci, and de-repression of cardiogenic gene expression during iCM conversion. Furthermore, Bmi1 deletion could substitute for Gata4 during iCM reprogramming. Thus, Bmi1 acts as a critical epigenetic barrier to iCM production. Bypassing this barrier simplifies iCM generation and increases yield, potentially streamlining iCM production for therapeutic purposes.
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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.