ArticleInternational journal of molecular medicine2015
Effects of miRNA-455 on cardiac hypertrophy induced by pressure overload.
Article in International journal of molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 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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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
19 citing papers in PubMed.
- Mitigation of Doxorubicin Cardiotoxicity With Synergistic miRNA Combinations Identified Using Combinatorial Genetics en masse (CombiGEM).JACC. CardioOncology · 2025Article
- miR-1183 Is a Key Marker of Remodeling upon Stretch and Tachycardia in Human Myocardium.International journal of molecular sciences · 2022Article
- MicroRNA-34c-5p provokes isoprenaline-induced cardiac hypertrophy by modulating autophagyActa pharmaceutica Sinica. B · 2022Article
- Potential Applications and Functional Roles of Exosomes in Cardiometabolic Disease.Pharmaceutics · 2021Review
- The titin N2B and N2A regions: biomechanical and metabolic signaling hubs in cross-striated muscles.Biophysical reviews · 2021Review
- miR-455-5p regulates atrial fibrillation by targeting suppressor of cytokines signaling 3.Journal of physiology and biochemistry · 2021Article
- Aging, MicroRNAs, and Heart Failure.Current problems in cardiology · 2020Review
- Analysis of extracellular vesicle miRNA profiles in heart failure.Journal of cellular and molecular medicine · 2020Article
- LncRNA promoted inflammatory response in ischemic heart failure through regulation of miR-455-3p/TRAF6 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Heat shock proteins and their expression in primary murine cardiac cell populations during ischemia and reperfusion.Molecular and cellular biochemistry · 2020Review
- MicroRNA-327 regulates cardiac hypertrophy and fibrosis induced by pressure overload.International journal of molecular medicine · 2018Article
- A Specific Circulating MicroRNA Cluster Is Associated to Late Differential Cardiac Response to Doxorubicin-Induced CardiotoxicityDisease markers · 2018Article
- Sexual dimorphism in the fetal cardiac response to maternal nutrient restriction.Journal of molecular and cellular cardiology · 2017Article
- Unfolded protein response plays a critical role in heart damage after myocardial ischemia/reperfusion in rats.PloS one · 2017Article
- MicroRNA as a Therapeutic Target in Cardiac Remodeling.BioMed research international · 2017Review
- Diagnostic and prognostic value of circulating microRNAs in heart failure with preserved and reduced ejection fraction.World journal of cardiology · 2015Review
- Article
- The Role of Estrogen in Cardiac Metabolism and Diastolic Function.Methodist DeBakey cardiovascular journalReview
- Cardiovascular Changes Associated with Hypertensive Heart Disease and Aging.Cell transplantationReview
Corrections and comments
- Retracted
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
microRNAs (miRNAs or miRs) are essential in cardiac hypertrophy and in the development of heart failure. In the present study, we aimed to determine whether the restoration of miRNA-455 (miR-455) gene expression in vivo aggravates hypertrophy, but protects against adverse cardiac remodeling induced by pressure overload. Cardiac hypertrophy was induced by left ventricular pressure overload in male mice subjected to transverse aortic constriction (TAC). The mice were randomly selected to receive a tail vein injection of either miR-455 or green fluorescent protein per animal at 1, 8, 15 and 21 days following surgery. Cardiac hypertrophy, function and remodeling were evaluated by echocardiography, catheterization, histological analysis and the examination of the expression of specific genes and cardiac apoptosis. TAC (2 weeks following surgery) resulted in significant cardiac hypertrophy, which was significantly aggravated by treatment with miR-455. However, miR-455 replacement therapy markedly reduced myocardial fibrosis and inhibited apoptosis, suggesting that this therapy can prevent maladaptive ventricular remodeling. miR-455 was also identified and validated to target calreticulin, a protein that is critical for cardiac development. The restoration of miR-455 gene expression may thus be a potential therapeutic strategy to reverse pressure-induced cardiac hypertrophy and prevent maladaptive cardiac remodeling through the regulation of miR-455 at different time points following hypertrophy.
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Registered trials
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