ArticleCirculation research2014
Loss of MicroRNA-155 protects the heart from pathological cardiac hypertrophy.
Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses 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.
The trial behind it
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
87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 162 citations in OpenAlex.
- Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024Pooled it
- Differences in the cargos and functions of exosomes derived from six cardiac cell types: a systematic review.Stem cell research & therapy · 2019Pooled it
- Plasma Circulating Extracellular RNAs in Left Ventricular Remodeling Post-Myocardial Infarction.EBioMedicine · 2018Trial
- The functional role of the circular RNA circCDR1as targeting SERCA2a in the progression of pathological cardiac hypertrophy and heart failure.Journal of translational medicine · 2026Article
- Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026Review
- Interpretation of the molecular mechanism and therapeutic potential of microRNA‑155 in cardiovascular and cerebrovascular diseases (Review).International journal of molecular medicine · 2026Review
- Review
- The role of miR-155 in cardiovascular diseases: Potential diagnostic and therapeutic targets.International journal of cardiology. Cardiovascular risk and prevention · 2025Review
- Wenyang Zhenshuai Granules inhibits cardiomyocyte apoptosis in chronic heart failure by regulating p38 MAPK signaling pathway through exosomal miR-155.Frontiers in pharmacology · 2025Article
- Bibliometric and visual analysis of miRNAs in heart diseases from 2004 to 2023.Frontiers in cardiovascular medicine · 2025Article
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- miR-31-5p suppresses myocardial hypertrophy by targeting Nfatc2ip.Journal of cellular and molecular medicine · 2024Article
- Circular RNA-circPan3 attenuates cardiac hypertrophy via miR-320-3p/HSP20 axis.Cellular & molecular biology letters · 2024Article
- Extracellular vesicular microRNAs and cardiac hypertrophy.Frontiers in endocrinology · 2024Review
- miR-455-5p promotes pathological cardiac remodeling via suppression of PRMT1-mediated Notch signaling pathway.Cellular and molecular life sciences : CMLS · 2023Article
- Diagnostic Performance of Serum MicroRNAs for ST-Segment Elevation Myocardial Infarction in the Emergency Department.Biomedicines · 2023Article
- miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach.International journal of molecular sciences · 2023Review
- Clinical Significance of MicroRNAs, Long Non-Coding RNAs, and CircRNAs in Cardiovascular Diseases.Cells · 2023Review
- SZC-6, a small-molecule activator of SIRT3, attenuates cardiac hypertrophy in mice.Acta pharmacologica Sinica · 2023Article
- Extracellular Vesicles and Pathological Cardiac Hypertrophy.Advances in experimental medicine and biology · 2023Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
rationaleIn response to mechanical and pathological stress, adult mammalian hearts often undergo mal-remodeling, a process commonly characterized as pathological hypertrophy, which is associated with upregulation of fetal genes, increased fibrosis, and reduction of cardiac dysfunction. The molecular pathways that regulate this process are not fully understood.
objectiveTo explore the function of microRNA-155 (miR-155) in cardiac hypertrophy and remodeling. METHODS AND
resultsOur previous work identified miR-155 as a critical microRNA that repressed the expression and function of the myocyte enhancer factor 2A. In this study, we found that miR-155 is expressed in cardiomyocytes and that its expression is reduced in pressure overload-induced hypertrophic hearts. In mouse models of cardiac hypertrophy, miR-155 null hearts suppressed cardiac hypertrophy and cardiac remodeling in response to 2 independent pathological stressors, transverse aortic restriction and an activated calcineurin transgene. Most importantly, loss of miR-155 prevents the progress of heart failure and substantially extends the survival of calcineurin transgenic mice. The function of miR-155 in hypertrophy is confirmed in isolated cardiomyocytes. We identified jumonji, AT rich interactive domain 2 (Jarid2) as an miR-155 target in the heart. miR-155 directly represses Jarid2, whose expression is increased in miR-155 null hearts. Inhibition of endogenous Jarid2 partially rescues the effect of miR-155 loss in isolated cardiomyocytes.
conclusionsOur studies uncover miR-155 as an inducer of pathological cardiomyocyte hypertrophy and suggest that inhibition of endogenous miR-155 might have clinical potential to suppress cardiac hypertrophy and heart failure.
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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.