ArticleRNA biology2017
Identification of miR-34 regulatory networks in settings of disease and antimiR-therapy: Implications for treating cardiac pathology and other diseases.
Article in RNA biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
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- Critical analysis of descriptive microRNA data in the translational research on cardioprotection and cardiac repair: lost in the complexity of bioinformatics.Basic research in cardiology · 2025Review
- IDMIR: identification of dysregulated miRNAs associated with disease based on a miRNA-miRNA interaction network constructed through gene expression data.Briefings in bioinformatics · 2024Article
- The roles of miRNAs in adult skeletal muscle satellite cells.Free radical biology & medicine · 2023Review
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- miRNA:miRNA Interactions: A Novel Mode of miRNA Regulation and Its Effect On Disease.Advances in experimental medicine and biology · 2022Article
- Identification of miRNA-34a and miRNA-155 as prognostic markers for mantle cell lymphoma.The Journal of international medical research · 2021Article
- miRNA interplay: mechanisms and consequences in cancer.Disease models & mechanisms · 2021Review
- Circulating MicroRNAs as Biomarkers of Accelerated Sarcopenia in Chronic Heart Failure.Global heart · 2021Article
- Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- LncRNA Tincr regulates PKCɛ expression in a miR-31-5p-dependent manner in cardiomyocyte hypertrophy.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- PD-1 inhibitor inducing exosomal miR-34a-5p expression mediates the cross talk between cardiomyocyte and macrophage in immune checkpoint inhibitor-related cardiac dysfunction.Journal for immunotherapy of cancer · 2020Article
- Discovery and Functional Prediction of Long Non-Coding RNAs Common to Ischemic Stroke and Myocardial Infarction.Journal of lipid and atherosclerosis · 2020Article
- Immune checkpoint inhibitor induces cardiac injury through polarizing macrophages via modulating microRNA-34a/Kruppel-like factor 4 signaling.Cell death & disease · 2020Article
- BMP10 preserves cardiac function through its dual activation of SMAD-mediated and STAT3-mediated pathways.The Journal of biological chemistry · 2019Article
- Noncoding RNAs regulating cardiac muscle mass.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Review
- The Genomic Origins of Small Mitochondrial RNAs: Are They Transcribed by the Mitochondrial DNA or by Mitochondrial Pseudogenes within the Nucleus (NUMTs)?Genome biology and evolution · 2019Article
- Effects of HIV-1 gp120 and TAT-derived microvesicles on endothelial cell function.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Downregulation of miR-34a promotes endothelial cell growth and suppresses apoptosis in atherosclerosis by regulating Bcl-2.Heart and vessels · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the miR-34 family (miR-34a, -34b, -34c) is elevated in settings of heart disease, and inhibition with antimiR-34a/antimiR-34 has emerged as a promising therapeutic strategy. Under chronic cardiac disease settings, targeting the entire miR-34 family is more effective than targeting miR-34a alone. The identification of transcription factor (TF)-miRNA regulatory networks has added complexity to understanding the therapeutic potential of miRNA-based therapies. Here, we sought to determine whether antimiR-34 targets secondary miRNAs via TFs which could contribute to antimiR-34-mediated protection. Using miRNA-Seq we identified differentially regulated miRNAs in hearts from mice with cardiac pathology due to transverse aortic constriction (TAC), and focused on miRNAs which were also regulated by antimiR-34. Two clusters of stress-responsive miRNAs were classified as "pathological" and "cardioprotective," respectively. Using ChIPBase we identified 45 TF binding sites on the promoters of "pathological" and "cardioprotective" miRNAs, and 5 represented direct targets of miR-34, with the capacity to regulate other miRNAs. Knockdown studies in a cardiomyoblast cell line demonstrated that expression of 2 "pathological" miRNAs (let-7e, miR-31) was regulated by one of the identified TFs. Furthermore, by qPCR we confirmed that expression of let-7e and miR-31 was lower in hearts from antimiR-34 treated TAC mice; this may explain why targeting the entire miR-34 family is more effective than targeting miR-34a alone. Finally, we showed that Acsl4 (a common target of miR-34, let-7e and miR-31) was increased in hearts from TAC antimiR-34 treated mice. In summary, antimiR-34 regulates the expression of other miRNAs and this has implications for drug development.
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