ArticleStem cell reports2014
miR-133a enhances the protective capacity of cardiac progenitors cells after myocardial infarction.
Article in Stem cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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.
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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
89 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Differences in the cargos and functions of exosomes derived from six cardiac cell types: a systematic review.Stem cell research & therapy · 2019Pooled it
- Impact ofJournal of cardiovascular development and disease · 2026Review
- Extracellular Vesicles in Cardiac Cell Crosstalk: from Intercellular Communication to Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Exercise-induced muscle exosomes: microRNA cargo as regulators of cardiovascular remodeling and disease progression.Journal of translational medicine · 2026Review
- Advances in MicroRNA-Based Therapies for Cardiac Repair: Emerging Strategies for Treating Myocardial Infarction.Molecular and cellular biochemistry · 2026Review
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- Oxidative Stress in Takotsubo Syndrome: Insights into Extracellular Vesicles and Their Potential Clinical Relevance.Antioxidants (Basel, Switzerland) · 2026Review
- Extracellular Vesicles in the Heart-Organ Axis: From Inter-Organ Communication to Precision Nanomedicine for Heart Diseases.International journal of nanomedicine · 2026Review
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Genistein Enhances the Beneficial Effects of Exercise on Antioxidant and Anti-inflammatory Balance and Cardiomyopathy in Ovariectomized Diabetic Rats.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2025Article
- Development of aInternational journal of molecular sciences · 2024Article
- Non-Coding Ribonucleic Acids as Diagnostic and Therapeutic Targets in Cardiac Fibrosis.Current heart failure reports · 2024Review
- The Roles of Exosome-Derived microRNAs in Cardiac Fibrosis.Molecules (Basel, Switzerland) · 2024Review
- Regulation mechanism of microRNAs in cardiac cells-derived exosomes in cell crosstalk.Frontiers in pharmacology · 2024Review
- Cardiac cells and mesenchymal stem cells derived extracellular vesicles: a potential therapeutic strategy for myocardial infarction.Frontiers in cardiovascular medicine · 2024Review
- Extracellular vesicular microRNAs and cardiac hypertrophy.Frontiers in endocrinology · 2024Review
- miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach.International journal of molecular sciences · 2023Review
- Modeling Cardiotoxicity in Pediatric Oncology Patients Using Patient-Specific iPSC-Derived Cardiomyocytes Reveals Downregulation of Cardioprotective microRNAs.Antioxidants (Basel, Switzerland) · 2023Article
- MicroRNA profiling in dogs undergoing induced ischemic heart infarction: An experimental study.Veterinary world · 2023Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vascularization and cardiomyocyte proliferation. The beneficial effects of miR-133a-CPCs seem to correlate with the upregulated expression of several relevant paracrine factors and the plausible cooperative secretion of miR-133a via exosomal transport. Finally, an in vitro heart muscle model confirmed the antiapoptotic effects of miR-133a-CPCs, favoring the structuration and contractile functionality of the artificial tissue.
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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.