ArticlePloS one2014
Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.
- A meta-analysis of microRNA expression profiling studies in heart failure.Heart failure reviews · 2021Pooled it
- micro-RNAs dependent regulation of DNMT and HIF1α gene expression in thrombotic disorders.Scientific reports · 2019Pooled it
- Diabetes mellitus disrupts lncRNA Malat1 regulation of cardiac mitochondrial genome-encoded protein expression.American journal of physiology. Heart and circulatory physiology · 2024Article
- Cardiomyopathies: The Role of Non-Coding RNAs.Non-coding RNA · 2024Review
- MicroRNA-30d and -483-3p for bi-ventricular remodelling and miR-126-3p for pulmonary hypertension in advanced heart failure.ESC heart failure · 2024Article
- Insight into the Inter-Organ Crosstalk and Prognostic Role of Liver-Derived MicroRNAs in Metabolic Disease Progression.Biomedicines · 2023Review
- The Role of MicroRNAs in Dilated Cardiomyopathy: New Insights for an Old Entity.International journal of molecular sciences · 2022Review
- Mitochondrial nucleoid in cardiac homeostasis: bidirectional signaling of mitochondria and nucleus in cardiac diseases.Basic research in cardiology · 2021Review
- Dietary restriction in the long-chain acyl-CoA dehydrogenase knockout mouse.Molecular genetics and metabolism reports · 2021Article
- Cardiac-specific overexpression of miR-122 induces mitochondria-dependent cardiomyocyte apoptosis and promotes heart failure by inhibiting Hand2.Journal of cellular and molecular medicine · 2021Article
- Exosomes in Cardiovascular Diseases: Pathological Potential of Nano-Messenger.Frontiers in cardiovascular medicine · 2021Review
- Circulating miRNAs as Potential Biomarkers Associated with Cardiac Remodeling and Fibrosis in Chagas Disease Cardiomyopathy.International journal of molecular sciences · 2019Article
- Association of intronic DNA methylation and hydroxymethylation alterations in the epigenetic etiology of dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Article
- MicroRNA-325-3p protects the heart after myocardial infarction by inhibiting RIPK3 and programmed necrosis in mice.BMC molecular biology · 2019Article
- Epigenetics in dilated cardiomyopathy.Current opinion in cardiology · 2019Review
- Epigenetics: a potential key mechanism involved in the pathogenesis of cardiorenal syndromes.Journal of nephrology · 2018Review
- Molecular mechanism of diabetic cardiomyopathy and modulation of microRNA function by synthetic oligonucleotides.Cardiovascular diabetology · 2018Review
- Circulating microRNA signature for the diagnosis of childhood dilated cardiomyopathy.Scientific reports · 2018Article
- Liver microRNAs: potential mediators and biomarkers for metabolic and cardiovascular disease?European heart journal · 2016Review
- Reversal of Phospholamban Inhibition of the Sarco(endo)plasmic Reticulum Ca2+-ATPase (SERCA) Using Short, Protein-interacting RNAs and Oligonucleotide Analogs.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) regulate many aspects of cellular function and their deregulation has been implicated in heart disease. MiRNA-30c is differentially expressed in the heart during the progression towards heart failure and in vitro studies hint to its importance in cellular physiology. As little is known about the in vivo function of miRNA-30c in the heart, we generated transgenic mice that specifically overexpress miRNA-30c in cardiomyocytes. We show that these mice display no abnormalities until about 6 weeks of age, but subsequently develop a severely dilated cardiomyopathy. Gene expression analysis of the miRNA-30c transgenic hearts before onset of the phenotype indicated disturbed mitochondrial function. This was further evident by the downregulation of mitochondrial oxidative phosphorylation (OXPHOS) complexes III and IV at the protein level. Taken together these data indicate impaired mitochondrial function due to OXPHOS protein depletion as a potential cause for the observed dilated cardiomyopathic phenotype in miRNA-30c transgenic mice. We thus establish an in vivo role for miRNA-30c in cardiac physiology, particularly in mitochondrial 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.