ArticlePLoS genetics2013
miR-1/133a clusters cooperatively specify the cardiomyogenic lineage by adjustment of myocardin levels during embryonic heart development.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Genetic and Epigenetic Factors of Takotsubo Syndrome: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Impact ofJournal of cardiovascular development and disease · 2026Review
- Advances in MicroRNA-Based Therapies for Cardiac Repair: Emerging Strategies for Treating Myocardial Infarction.Molecular and cellular biochemistry · 2026Review
- Maternal-fetal microRNA axis in congenital heart disease: implications for tetralogy of Fallot.Frontiers in cardiovascular medicine · 2026Review
- Advances in miRNA research: Unraveling the complexities of gene regulation.Animal models and experimental medicine · 2025Review
- Absolute quantification of mammalian microRNAs for therapeutic RNA cleavage and detargeting.RNA (New York, N.Y.) · 2025Article
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- miR-1 as a Key Epigenetic Regulator in Early Differentiation of Cardiac Sinoatrial Region.International journal of molecular sciences · 2024Article
- Dgcr8 functions in the secondary heart field for outflow tract and right ventricle development in mammals.Developmental biology · 2024Article
- Trials and Tribulations of MicroRNA Therapeutics.International journal of molecular sciences · 2024Review
- miR-195b is required for proper cellular homeostasis in the elderly.Scientific reports · 2024Article
- Influence of Maternal BLV Infection on miRNA and tRF Expression in Calves.Pathogens (Basel, Switzerland) · 2023Article
- Cardiac microRNAs: diagnostic and therapeutic potential.Archives of medical science : AMS · 2023Article
- The negative regulation of gene expression by microRNAs as key driver of inducers and repressors of cardiomyocyte differentiation.Clinical science (London, England : 1979) · 2022Review
- Circulating microRNAs predispose to takotsubo syndrome following high-dose adrenaline exposure.Cardiovascular research · 2022Article
- Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function.Nature communications · 2022Article
- Repression ofScience advances · 2021Article
- Direct Reprogramming of Cardiac Fibroblasts to Repair the Injured Heart.Journal of cardiovascular development and disease · 2021Review
- miRNA in cardiac development and regeneration.Cell regeneration (London, England) · 2021Review
- The roles of microRNAs in mouse development.Nature reviews. Genetics · 2021Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
miRNAs are small RNAs directing many developmental processes by posttranscriptional regulation of protein-coding genes. We uncovered a new role for miR-1-1/133a-2 and miR-1-2/133a-1 clusters in the specification of embryonic cardiomyocytes allowing transition from an immature state characterized by expression of smooth muscle (SM) genes to a more mature fetal phenotype. Concomitant knockout of miR-1-1/133a-2 and miR-1-2/133a-1 released suppression of the transcriptional co-activator myocardin, a major regulator of SM gene expression, but not of its binding partner SRF. Overexpression of myocardin in the embryonic heart essentially recapitulated the miR-1/133a mutant phenotype at the molecular level, arresting embryonic cardiomyocytes in an immature state. Interestingly, the majority of postulated miR-1/133a targets was not altered in double mutant mice, indicating that the ability of miR-1/133a to suppress target molecules strongly depends on the cellular context. Finally, we show that myocardin positively regulates expression of miR-1/133a, thus constituting a negative feedback loop that is essential for early cardiac development.
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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.