ArticleJournal of cardiovascular pharmacology2017
MiR-30e Attenuates Isoproterenol-induced Cardiac Fibrosis Through Suppressing Snai1/TGF-β Signaling.
Article in Journal of cardiovascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- A comprehensive study on the impact ofFrontiers in cardiovascular medicine · 2025Article
- Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction.International journal of molecular sciences · 2024Article
- Puerarin inhibits NHE1 activity by interfering with the p38 pathway and attenuates mitochondrial damage induced by myocardial calcium overload in heart failure rats.Acta biochimica et biophysica Sinica · 2024Article
- Preventive and treatment efficiency of dendrosomal nano-curcumin against ISO-induced cardiac fibrosis in mouse model.PloS one · 2024Article
- Article
- miR-31-5p-Modified RAW 264.7 Macrophages Affect Profibrotic Phenotype of Lymphatic Endothelial Cells In Vitro.International journal of molecular sciences · 2022Article
- Exosomes: mediators regulating the phenotypic transition of vascular smooth muscle cells in atherosclerosis.Cell communication and signaling : CCS · 2022Review
- Diagnostic and Therapeutic Properties of Exosomes in Cardiac Fibrosis.Frontiers in cell and developmental biology · 2022Review
- miRNAs in decidual NK cells: regulators worthy of attention during pregnancy.Reproductive biology and endocrinology : RB&E · 2021Review
- MicroRNAs-The Heart of Post-Myocardial Infarction Remodeling.Diagnostics (Basel, Switzerland) · 2021Review
- MicroRNA‑331 inhibits isoproterenol‑induced expression of profibrotic genes in cardiac myofibroblasts via the TGFβ/smad3 signaling pathway.Scientific reports · 2021Article
- hsa-miR-4443 inhibits myocardial fibroblast proliferation by targeting THBS1 to regulate TGF-β1/α-SMA/collagen signaling in atrial fibrillation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- The cardioprotective effects of the new crystal form of puerarin in isoproterenol-induced myocardial ischemia rats based on metabolomics.Scientific reports · 2020Article
- MicroRNA-30e regulates TGF-β-mediated NADPH oxidase 4-dependent oxidative stress by Snai1 in atherosclerosis.International journal of molecular medicine · 2019Article
- HIF-1 regulation of miR-29c impairs SERCA2 expression and cardiac contractility.American journal of physiology. Heart and circulatory physiology · 2019Article
- Comparison of Cardiac miRNA Transcriptomes Induced by Diabetes and Rapamycin Treatment and Identification of a Rapamycin-Associated Cardiac MicroRNA Signature.Oxidative medicine and cellular longevity · 2018Article
- Geniposide Alleviates Isoproterenol-Induced Cardiac Fibrosis Partially via SIRT1 ActivationFrontiers in pharmacology · 2018Article
- MicroRNA-495 inhibits the high glucose-induced inflammation, differentiation and extracellular matrix accumulation of cardiac fibroblasts through downregulation of NOD1.Cellular & molecular biology letters · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNAs are a class of small RNA molecules that inhibit protein expression through either degradation of messenger RNA or interference with protein translation. Our previous work suggested an involvement of miR-30e in myocardial fibrosis; however, the exact role of miR-30e in the pathogenesis of cardiac fibrosis and the underlying mechanisms are not known.
methodsMale Sprague Dawley rats were treated with isoproterenol (ISO) to induce cardiac remodeling and fibrosis and treated with either miR-30e agomir (AG) or antagomir and respective controls. The expression of miR-30e was evaluated by reverse transcription and quantitative polymerase chain reaction. Myocardial fibrosis was assessed by Masson's trichrome staining, and the level of oxidative stress and the expression of Snai1 and transforming growth factor-beta (TGF-β) were detected using Western blots.
resultsA significant downregulation of miR-30e was found in the hearts of ISO-treated rats with cardiac fibrosis compared with nontreated controls. In vivo administration of miR-30e AG increased the survival of ISO-treated rats compared with AG-negative control administration, which was associated with reduced oxidative stress. We further identified Snai1 as a novel miR-30e target. Snai1 expression was significantly increased in hearts from ISO-treated rats, which coincided with decreased miR-30e expression and increased TGF-β expression. An miR-30e putative target sequence was identified in the 3'-untranslated region (UTR) Snai1. In a reporter assay, miR-30e greatly suppressed the activity of wild-type 3'-UTR-fused luciferase reporter, but showed no significant effect with the mutated 3'-UTR-fused reporter.
conclusionMiR-30e attenuated ISO-induced cardiac dysfunction and cardiac fibrosis in a rat cardiac remodeling model. Mechanistically, miR-30e suppressed Snai1/TGF-β pathway which was involved in ISO-induced cardiac remodeling.
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