ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Long Noncoding RNA (lncRNA) n379519 Promotes Cardiac Fibrosis in Post-Infarct Myocardium by Targeting miR-30.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. 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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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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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Non-coding RNA-mediated epigenetic alterations in Grave's ophthalmopathy: A scoping systematic review.Non-coding RNA research · 2023Article
- Clinical Significance of MicroRNAs, Long Non-Coding RNAs, and CircRNAs in Cardiovascular Diseases.Cells · 2023Review
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- Non-coding RNAs in human health and disease: potential function as biomarkers and therapeutic targets.Functional & integrative genomics · 2023Review
- New Insights into the Functions of MicroRNAs in Cardiac Fibrosis: From Mechanisms to Therapeutic Strategies.Genes · 2022Review
- lncRNA Vgll3 Regulates the Activated Proliferation of Mouse Myocardial Fibroblasts through TGF-BioMed research international · 2022Article
- TUG1 knockdown suppresses cardiac fibrosis after myocardial infarction.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
- Long Non-Coding RNAs in Cardiovascular Diseases: Potential Function as Biomarkers and Therapeutic Targets of Exercise Training.Non-coding RNA · 2021Review
- Therapies Targeted at Non-Coding RNAs in Prevention and Limitation of Myocardial Infarction and Subsequent Cardiac Remodeling-Current Experience and Perspectives.International journal of molecular sciences · 2021Review
- Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics.Frontiers in genetics · 2021Review
- Long Non-Coding RNAs in Atrial Fibrillation: Pluripotent Stem Cell-Derived Cardiomyocytes as a Model System.International journal of molecular sciences · 2020Review
- TGF-β and WNT signaling pathways in cardiac fibrosis: non-coding RNAs come into focus.Cell communication and signaling : CCS · 2020Review
- miRNAs and lncRNAs inInternational journal of molecular sciences · 2020Review
- Regulation of Long Non-coding RNAs and MicroRNAs in Heart Disease: Insight Into Mechanisms and Therapeutic Approaches.Frontiers in physiology · 2020Review
- Long Non-Coding RNA 554 Promotes Cardiac Fibrosis via TGF-β1 Pathway in Mice Following Myocardial Infarction.Frontiers in pharmacology · 2020Article
- LncRNA HCG11 Suppresses Cell Proliferation and Promotes Apoptosis via Sponging miR-224-3p in Non-Small-Cell Lung Cancer Cells.OncoTargets and therapy · 2020Article
- Age-Related Pathways in Cardiac Regeneration: A Role for lncRNAs?Frontiers in physiology · 2020Review
- Upregulation of lncRNA RMRP promotes the activation of cardiac fibroblasts by regulating miR‑613.Molecular medicine reports · 2019Article
- The microRNA in ventricular remodeling: the miR-30 family.Bioscience reports · 2019Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Abnormally expressed long noncoding RNAs (lncRNAs) are recognized as one of the key causes of cardiac diseases. However, the role of lncRNA in cardiac fibrosis remains largely unknown. MATERIAL AND METHODS The experiment was divided into 4 groups: a sham operation group, a myocardial infarction (MI) group, a lentivirus group (LV-si-n379519), and a lentivirus control (LV-NC) group. The adenovirus expression vectors LV-si-n379519 and LV-NC were constructed and transfected into mice. Echocardiography, HE staining, and Masson staining were performed to detect the heart function and collagen volume fraction in each group. RT-PCR was used to detect the expression level of n379519, miR-30, collagen I, and collagen III. In vitro, cardiac fibroblasts (CFs) were cultured and the relationship between n379519 and miR-30 was verified using luciferase reporter vector, n379519 siRNA, and miR-30 inhibitor. RESULTS The expression of n379519 was markedly upregulated in the hearts of mice with MI and in the fibrotic CFs. Knockdown of endogenous n379519 by its siRNA improved the heart function and reduced collagen deposition and the process of cardiac fibrosis. Further experiments showed the opposite trend of expression between n379519 and miR-30. Bioinformatics analysis and luciferase reporter assay indicated that n379519 directly binds to miR-30. Moreover, miR-30 inhibitor abrogated the collagen synthesis inhibition induced by n379519. CONCLUSIONS These findings reveal a novel function of n379519-miR-30 axis as a negative regulator for the treatment of MI-induced cardiac fibrosis and the associated cardiac dysfunction.
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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.