ArticleNature genetics2015
Trbp regulates heart function through microRNA-mediated Sox6 repression.
Article in Nature genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- The role of non-coding RNAs derived from macrophage exosomes in cardiovascular diseases.The Journal of physiology · 2026Review
- Integrated analysis of MYH6, MYH7, and MYH7B expression and their associated microRNAs in human end-stage heart failure.Frontiers in cardiovascular medicine · 2026Article
- Gut Microbiota and Bacterial Extracellular Vesicles: Emerging Roles in Myocardial Remodelling and Cardiac Health.Journal of extracellular biology · 2025Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Trbp inhibits cardiac fibrosis through TGF-β pathway-mediated cross-talk between cardiomyocytes and fibroblasts.Clinical science (London, England : 1979) · 2025Article
- Article
- Two-motif model illuminates DICER cleavage preferences.Nucleic acids research · 2024Article
- Effect of miR-499-5p/SOX6 axis on atrial fibrosis in rats with atrial fibrillation.Open medicine (Warsaw, Poland) · 2023Article
- Counteraction of Myocardial Ferritin Heavy Chain Deficiency by Heme Oxygenase-1.International journal of molecular sciences · 2022Article
- Sox6, A Potential Target for MicroRNAs in Cardiometabolic Disease.Current hypertension reports · 2022Review
- Cardiac CIP protein regulates dystrophic cardiomyopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Modulation of MicroRNA Processing by Dicer via Its Associated dsRNA Binding Proteins.Non-coding RNA · 2021Review
- The SRSF4-GAS5-Glucocorticoid Receptor Axis Regulates Ventricular Hypertrophy.Circulation research · 2021Article
- LncRNA LncHrt preserves cardiac metabolic homeostasis and heart function by modulating the LKB1-AMPK signaling pathway.Basic research in cardiology · 2021Article
- Circular RNA circMYBPC1 promotes skeletal muscle differentiation by targeting MyHC.Molecular therapy. Nucleic acids · 2021Article
- miR-208a in Cardiac Hypertrophy and Remodeling.Frontiers in cardiovascular medicine · 2021Review
- Emerging roles of Sox6 in the renal and cardiovascular system.Physiological reports · 2020Review
- Intercalated disc protein Xinβ is required for Hippo-YAP signaling in the heart.Nature communications · 2020Article
- Human umbilical cord mesenchymal stem cells-derived exosomes transfers microRNA-19a to protect cardiomyocytes from acute myocardial infarction by targeting SOX6.Cell cycle (Georgetown, Tex.) · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiomyopathy is associated with altered expression of genes encoding contractile proteins. Here we show that Trbp (Tarbp2), an RNA-binding protein, is required for normal heart function. Cardiac-specific inactivation in mice of Trbp (Trbp(cKO)) caused progressive cardiomyopathy and lethal heart failure. Loss of Trbp function resulted in upregulation of Sox6, repression of genes encoding normal cardiac slow-twitch myofiber proteins and pathologically increased expression of genes encoding skeletal fast-twitch myofiber proteins. Remarkably, knockdown of Sox6 fully rescued the Trbp-mutant phenotype, whereas mice overexpressing Sox6 phenocopied Trbp(cKO) mice. Trbp inactivation was mechanistically linked to Sox6 upregulation through altered processing of miR-208a, which is a direct inhibitor of Sox6. Transgenic overexpression of Mir208a sufficiently repressed Sox6, restored the balance in gene expression for fast- and slow-twitch myofiber proteins, and rescued cardiac function in Trbp(cKO) mice. Together, our studies identify a new Trbp-mediated microRNA-processing mechanism in the regulation of a linear genetic cascade essential for normal heart function.
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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.