ArticleeLife2013
microRNA-1 regulates sarcomere formation and suppresses smooth muscle gene expression in the mammalian heart.
Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 113 citations in OpenAlex.
- Non-Coding RNAs from Cardiac Development to Disease: Regulatory Context, Regenerative Potential, and Translational Limits.International journal of molecular sciences · 2026Review
- Impact ofJournal of cardiovascular development and disease · 2026Review
- Review
- Maternal Blood as a Window to the Fetal Heart: Novel Biomarkers for Early Detection of Septal Defects.Biomedicines · 2026Review
- Cooked meat-derived extracellular vesicles ssc-miR-1 induces metabolic disorders in the mice liver via PI3k/AKT pathway.NPJ science of food · 2026Article
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Long-term impact of anthracycline in early-stage breast cancer, bridging of MiRNAs profiler for early cardiotoxicity.Cardio-oncology (London, England) · 2025Article
- RNA signaling in skeletal muscle: the central role of microRNAs and exosomal microRNAs.Frontiers in cell and developmental biology · 2025Review
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- miR-26 Deficiency Causes Alterations in Lens Transcriptome and Results in Adult-Onset Cataract.Investigative ophthalmology & visual science · 2024Article
- miR-26 deficiency causes alterations in lens transcriptome and results in adult-onset cataract.bioRxiv : the preprint server for biology · 2024Article
- MicroRNA-1 Deficiency Is a Primary Etiological Factor Disrupting Cardiac Contractility and Electrophysiological Homeostasis.Circulation. Arrhythmia and electrophysiology · 2024Article
- Review
- Knockdown of deleterious miRNA in progenitor cell-derived small extracellular vesicles enhances tissue repair in myocardial infarction.Science advances · 2023Article
- Association of Genetic Polymorphisms and Serum Levels of miR-1-3p with Postoperative Mortality following Abdominal Aortic Aneurysm Repair.Journal of clinical medicine · 2023Article
- Cardiac microRNAs: diagnostic and therapeutic potential.Archives of medical science : AMS · 2023Article
- miRNA-1 promotes acute myeloid leukemia cell pathogenesis through metabolic regulation.Frontiers in genetics · 2023Article
- Sarcomere maturation: function acquisition, molecular mechanism, and interplay with other organelles.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function.Nature communications · 2022Article
- miR-1 sustains muscle physiology by controlling V-ATPase complex assembly.Science advances · 2021Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
microRNA-1 (miR-1) is an evolutionarily conserved, striated muscle-enriched miRNA. Most mammalian genomes contain two copies of miR-1, and in mice, deletion of a single locus, miR-1-2, causes incompletely penetrant lethality and subtle cardiac defects. Here, we report that deletion of miR-1-1 resulted in a phenotype similar to that of the miR-1-2 mutant. Compound miR-1 knockout mice died uniformly before weaning due to severe cardiac dysfunction. miR-1-null cardiomyocytes had abnormal sarcomere organization and decreased phosphorylation of the regulatory myosin light chain-2 (MLC2), a critical cytoskeletal regulator. The smooth muscle-restricted inhibitor of MLC2 phosphorylation, Telokin, was ectopically expressed in the myocardium, along with other smooth muscle genes. miR-1 repressed Telokin expression through direct targeting and by repressing its transcriptional regulator, Myocardin. Our results reveal that miR-1 is required for postnatal cardiac function and reinforces the striated muscle phenotype by regulating both transcriptional and effector nodes of the smooth muscle gene expression network. DOI: http://dx.doi.org/10.7554/eLife.01323.001.
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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.