ArticleCirculation2023
Direct Reprogramming Improves Cardiac Function and Reverses Fibrosis in Chronic Myocardial Infarction.
Article in Circulation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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.
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Who cites it
87 citing papers in PubMed, 117 citations in OpenAlex.
- Human induced pluripotent stem cell-derived cardiomyocyte patch enhances cardiac regeneration in a J2N-k hamster model of dilated cardiomyopathy.Regenerative therapy · 2026Article
- Role of ATOH8 in Mitigating Cardiac Fibrosis in Heart Failure via Inhibition of the Transcriptional Repression of Smad7 by RUNX2.Biomolecules & therapeutics · 2026Article
- SerpinA3 is an Endogenous TGF-β Receptor Antagonist that Attenuates Cardiac Fibroblast Activation and Fibrotic Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bazedoxifene Attenuates Isoproterenol-Induced Cardiac Fibroblast Activation and Fibrotic Phenotype via Modulation of the IL-6/STAT3 Signaling Axis.Current issues in molecular biology · 2026Article
- CD22Science China. Life sciences · 2026Article
- ZEB2 SUMOylation in Cardiac Fibroblast Drives Post-Infarction Cardiac Remodeling through CtBP1-Associated repression of Nr4a1.iScience · 2026Article
- Biomaterial-Assisted Stem Cell Therapy and Exosome Delivery in Myocardial Infarction: A Narrative Review.Biomimetics (Basel, Switzerland) · 2026Review
- Sulfotransferase signaling sustains fibroblast identity and antagonizes therapeutic cardiac reprogramming.Nature communications · 2026Article
- Cardiac regeneration and repair: the emerging mechanisms and therapeutic approaches.Molecular biomedicine · 2026Review
- Psoralen enhances direct cardiac reprogramming via activating PPARα and driving mitochondrial fission and improves cardiac function after myocardial infarction.Stem cell research & therapy · 2026Article
- In silico predictions of action potential propagation in doxorubicin cardiotoxicity: A parametric study using preclinical 3D magnetic resonance imaging-based fibrotic left ventricle models.The Journal of physiology · 2026Article
- Iminostilbene, a Carbamazepine Intermediate, Alleviates Myocardial Fibrosis after Myocardial Infarction via Targeting Galectin3.ACS pharmacology & translational science · 2026Article
- Electrical coupling between transplanted cardiomyocytes and host myocardium to prevent arrhythmia.Disease models & mechanisms · 2026Review
- RelJournal of translational medicine · 2026Article
- Beyond Reperfusion: Early Molecular Drivers and Therapeutic Opportunities in Acute Post-Infarction Cardiac Fibrosis.International journal of molecular sciences · 2026Review
- Matrifibrocytes Redefine Cardiac Fibrosis: From Terminal Differentiation to Translational Modulation.Journal of cellular and molecular medicine · 2026Review
- Glabridin improves cardiac remodeling after myocardial infarction by activating PPARγ to regulate the ubiquitination and degradation of EGFR.Biology direct · 2026Article
- Inhibition ofPediatric discovery · 2026Article
- The Role of MEF2 in Scar Formation and Angiogenesis.Journal of cosmetic dermatology · 2026Review
- Leptin Activates Brain-BAT-Heart Crosstalk to Promote Cardiac Protection.Circulation research · 2026Article
27 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBecause adult cardiomyocytes have little regenerative capacity, resident cardiac fibroblasts (CFs) synthesize extracellular matrix after myocardial infarction (MI) to form fibrosis, leading to cardiac dysfunction and heart failure. Therapies that can regenerate the myocardium and reverse fibrosis in chronic MI are lacking. The overexpression of cardiac transcription factors, including
methodsWe generated a novel Tcf21
resultsWe confirmed the efficacy of transgenic in vitro and in vivo cardiac reprogramming for acute MI. In chronic MI, in vivo cardiac reprogramming converted ≈2% of resident CFs into iCMs, in which a majority of iCMs were generated by means of bona fide cardiac reprogramming rather than by fusion with cardiomyocytes. Cardiac reprogramming significantly improved myocardial contraction and reduced fibrosis in chronic MI. Microarray analyses revealed that the overexpression of MGTH activated cardiac program and concomitantly suppressed fibroblast and inflammatory signatures in chronic MI. Single-cell RNA sequencing demonstrated that resident CFs consisted of 7 subclusters, in which the profibrotic CF population increased under chronic MI. Cardiac reprogramming suppressed fibroblastic gene expression in chronic MI by means of conversion of profibrotic CFs to a quiescent antifibrotic state. MGTH overexpression induced antifibrotic effects partly by suppression of Meox1, a central regulator of fibroblast activation.
conclusionsThese results demonstrate that cardiac reprogramming could repair chronic MI by means of myocardial regeneration and reduction of fibrosis. These findings present opportunities for the development of new therapies for chronic MI and heart failure.
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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.