ArticleCirculation research2019
Transient Introduction of miR-294 in the Heart Promotes Cardiomyocyte Cell Cycle Reentry After Injury.
Article in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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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
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- The expression profiles and roles of microRNAs in cardiac glucose metabolism.Frontiers in endocrinology · 2025Pooled it
- Lachnospiraceae-Derived Extracellular Vesicles Mediate the Cardioprotective Effects of Barley Leaf in Myocardial Infarction by Improving Intestinal Stem Cell Function.Journal of extracellular vesicles · 2026Article
- Activation of developmental transcription factors using RNA technology promotes heart repair.bioRxiv : the preprint server for biology · 2026Article
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Gene therapy in cardiac and vascular diseases: a review of approaches to treat genetic and common cardiovascular diseases with novel gene-based therapeutics.Cardiovascular research · 2025Review
- Maternal plasma microRNAs as potential biomarkers for triaging pregnancies of unknown location and ectopic pregnancy diagnosis.Non-coding RNA research · 2025Article
- Metabolic Disturbances Involved in Cardiovascular Diseases: The Role of Mitochondrial Dysfunction, Altered Bioenergetics and Oxidative Stress.International journal of molecular sciences · 2025Review
- Muscle-specific miR-499-5p delivered by small extracellular vesicles impairs endothelial function and ischemic hindlimb recovery in diabetic mice.Cardiovascular diabetology · 2025Article
- Critical analysis of descriptive microRNA data in the translational research on cardioprotection and cardiac repair: lost in the complexity of bioinformatics.Basic research in cardiology · 2025Review
- Foxk1 and Foxk2 promote cardiomyocyte proliferation and heart regeneration.Nature communications · 2025Article
- Delayed miR-199a Administration After Myocardial Infarction Precludes Pro-Regenerative Effects.JACC. Basic to translational science · 2025Article
- The highly conserved PIWI-interacting RNA CRAPIR antagonizes PA2G4-mediated NF110-NF45 disassembly to promote heart regeneration in mice.Nature cardiovascular research · 2025Article
- Engineered Cardiac Tissues as a Platform for CRISPR-Based Mitogen Discovery.Advanced healthcare materials · 2025Article
- Regenerative therapies for myocardial infarction: exploring the critical role of energy metabolism in achieving cardiac repair.Frontiers in cardiovascular medicine · 2025Review
- Efficacy of mesenchymal stem cells in treating tracheoesophageal fistula via the TLR4/NF-κb pathway in beagle macrophages.Heliyon · 2024Article
- m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Tailoring Treatment in Cardiovascular Diseases: The Role of Targeted Therapies.Pharmaceutics · 2024Review
- Cardiac regeneration: Pre-existing cardiomyocyte as the hub of novel signaling pathway.Genes & diseases · 2024Review
- Review
- Integrated small RNA, mRNA and protein omics reveal a miRNA network orchestrating metabolic maturation of the developing human heart.BMC genomics · 2023Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
Abstract
rationaleEmbryonic heart is characterized of rapidly dividing cardiomyocytes required to build a working myocardium. Cardiomyocytes retain some proliferative capacity in the neonates but lose it in adulthood. Consequently, a number of signaling hubs including microRNAs are altered during cardiac development that adversely impacts regenerative potential of cardiac tissue. Embryonic stem cell cycle miRs are a class of microRNAs exclusively expressed during developmental stages; however, their effect on cardiomyocyte proliferation and heart function in adult myocardium has not been studied previously.
objectiveTo determine whether transient reintroduction of embryonic stem cell cycle miR-294 promotes cardiomyocyte cell cycle reentry enhancing cardiac repair after myocardial injury. METHODS AND
resultsmiR-294 is expressed in the heart during development, prenatal stages, lost in the neonate, and adult heart confirmed by qRT-PCR and in situ hybridization. Neonatal ventricular myocytes treated with miR-294 showed elevated expression of Ki67, p-histone H3, and Aurora B confirmed by immunocytochemistry compared with control cells. miR-294 enhanced oxidative phosphorylation and glycolysis in Neonatal ventricular myocytes measured by seahorse assay. Mechanistically, miR-294 represses Wee1 leading to increased activity of the cyclin B1/CDK1 complex confirmed by qRT-PCR and immunoblot analysis. Next, a doxycycline-inducible AAV9-miR-294 vector was delivered to mice for activating miR-294 in myocytes for 14 days continuously after myocardial infarction. miR-294-treated mice significantly improved left ventricular functions together with decreased infarct size and apoptosis 8 weeks after MI. Myocyte cell cycle reentry increased in miR-294 hearts analyzed by Ki67, pH3, and AurB (Aurora B kinase) expression parallel to increased small myocyte number in the heart. Isolated adult myocytes from miR-294 hearts showed increased 5-ethynyl-2'-deoxyuridine+ cells and upregulation of cell cycle markers and miR-294 targets 8 weeks after MI.
conclusionsEctopic transient expression of miR-294 recapitulates developmental signaling and phenotype in cardiomyocytes promoting cell cycle reentry that leads to augmented cardiac function in mice after myocardial infarction.
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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.