ArticleBMC molecular biology2019
MiR-32-5p influences high glucose-induced cardiac fibroblast proliferation and phenotypic alteration by inhibiting DUSP1.
Article in BMC molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Pooled it
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- The Key Role and Mechanism of Oxidative Stress in Hypertrophic Cardiomyopathy: A Systematic Exploration Based on Multi-Omics Analysis and Experimental Validation.Antioxidants (Basel, Switzerland) · 2025Article
- Mechanism and research progress of MAPK signaling pathway in myocardial fibrosis.Frontiers in cardiovascular medicine · 2025Review
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- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- Triply Enhanced Immunotherapy via Dual Glycan Reforming Integrated with Perforation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Circulating microRNAs and cardiomyocyte proliferation in heart failure patients related to 10 years survival.ESC heart failure · 2023Article
- Role of single-cell ferroptosis regulation in intercellular communication and skin cutaneous melanoma progression and immunotherapy.Cancer immunology, immunotherapy : CII · 2023Article
- Noncoding RNAs: Master Regulator of Fibroblast to Myofibroblast Transition in Fibrosis.International journal of molecular sciences · 2023Review
- Histone methylation-mediated microRNA-32-5p down-regulation in sensory neurons regulates pain behaviors via targeting Cav3.2 channels.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- MiR-34a-3p suppresses pulmonary vascular proliferation in acute pulmonary embolism rat by targeting DUSP1.Bioscience reports · 2022Article
- TheGenes · 2022Article
- Article
- Article
- Magic and mystery of microRNA-32.Journal of cellular and molecular medicine · 2021Review
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Exosomal miR-365a-5p derived from HUC-MSCs regulates osteogenesis in GIONFH through the Hippo signaling pathway.Molecular therapy. Nucleic acids · 2021Article
- Acupuncture therapy protects PCOS patients with diabetes by regulating miR-32-3p/PLA2G4A pathway.American journal of translational research · 2021Article
- Multi-Omics Identifies Circulating miRNA and Protein Biomarkers for Facioscapulohumeral Dystrophy.Journal of personalized medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe current study aimed to investigate the effects of miR-32-5p on cardiac fibroblasts (CFs) that were induced with high levels of glucose; we also aimed to identify the potential mechanisms involved in the regulation of DUSP1 expression.
methodsHuman CFs were transfected with a miR-32-5p inhibitor or mimic and were treated with a normal concentration or a high concentration of glucose. Flow cytometry analysis was performed to identify cardiac fibroblasts by examining vimentin, fibronectin (FN) and α-actin expression in human CFs. qRT-PCR and western blot assays were performed to confirm the expression of miR-32-5p, DUSP1 and cardiac fibrosis relevant proteins. The proliferation of CFs was assessed by using MTT assay. An immunocytofluorescent staining assay was performed to determine the protein level of α-SMA and to investigate the degree of phenotypic changes in human CFs. The specific relationship between miR-32-5p and DUSP1 was investigated by a dual luciferase reporter assay. Cell apoptosis rates were measured with flow cytometry and the annexin V-FITC and propidine iodide (PI) staining method.
resultsA luciferase reporter assay indicated that miR-32-5p could directly target DUSP1. High glucose levels resulted in the overexpression of miR-32-5p, which downregulated DUSP1 expression. Both the upregulation of miR-32-5p and the downregulation of DUSP1 promoted cell apoptosis, proliferation and phenotypic changes in human CFs.
conclusionsAll findings in this study provide further evidence for the positive effects of miR-32-5p on cell proliferation and the phenotypic changes in CFs by inhibiting DUSP1 expression, and reveal that miR-32-5p could serve as prognostic diagnostic target for cardiac fibrosis.
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