Full metadata record
DC Field | Value | Language |
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dc.creator | Silveira-Assmann, T. (Taís) | - |
dc.creator | Milagro-Yoldi, F.I. (Fermín Ignacio) | - |
dc.creator | Martinez, J.A. (José Alfredo) | - |
dc.date.accessioned | 2021-09-23T08:13:11Z | - |
dc.date.available | 2021-09-23T08:13:11Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Silveira-Assmann, T. (Taís); Milagro-Yoldi, F.I. (Fermín Ignacio); Martinez, J.A. (José Alfredo). "Crosstalk between microRNAs, the putative target genes and the lncRNA network in metabolic diseases". Molecular Medicine Reports. 20 (4), 2019, 3543 - 3554 | es_ES |
dc.identifier.issn | 1791-2997 | - |
dc.identifier.other | PMID: 31485667 | - |
dc.identifier.uri | https://hdl.handle.net/10171/62044 | - |
dc.description.abstract | MicroRNAs (miRNAs/miRs) are small non‑coding RNAs (ncRNAs) that regulate gene expression. Emerging knowledge has suggested that miRNAs have a role in the pathogenesis of metabolic disorders, supporting the hypothesis that miRNAs may represent potential biomarkers or targets for this set of diseases. However, the current evidence is often controversial. Therefore, the aim of the present study was to determine the associations between miRNAs‑target genes, miRNA‑long ncRNAs (lncRNAs), and miRNAs‑small molecules in human metabolic diseases, including obesity, type 2 diabetes and non‑alcoholic fatty liver disease. The metabolic disease‑related miRNAs were obtained from the Human MicroRNA Disease Database (HMDD) and miR2Disease database. A search on the databases Matrix Decomposition and Heterogeneous Graph Inference (MDHGI) and DisGeNET were also performed. miRNAs target genes were obtained from three independent sources: Microcosm, TargetScan and miRTarBase. The interactions between miRNAs‑lncRNA and miRNA‑small molecules were performed using the miRNet web tool. The network analyses were performed using Cytoscape software. As a result, a total of 20 miRNAs were revealed to be associated with metabolic disorders in the present study. Notably, 6 miRNAs (miR‑17‑5p, miR‑29c‑3p, miR‑34a‑5p, miR‑103a‑3p, miR‑107 and miR‑132‑3p) were found in the four resources (HMDD, miR2Disease, MDHGI, and DisGeNET) used for these analyses, presenting a stronger association with the diseases. Furthermore, the target genes of these miRNAs participate in several pathways previously associated with metabolic diseases. In addition, interactions between miRNA‑lncRNA and miRNA‑small molecules were also found, suggesting that some molecules can modulate gene expression via such an indirect way. Thus, the results of this data mining and integration analysis provide further information on the possible molecular basis of the metabolic disease pathogenesis as well as provide a path to search for potential biomarkers and therapeutic targets concerning metabolic diseases. | es_ES |
dc.description.sponsorship | TSA is a recipient of scholarships from Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES; grant no. 88881.170123/2018-01). The present study was also supported by CIBERobn (grant no. CB12/03/30002). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Spandidos Publications | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.subject | Materias Investigacion::Ciencias de la Salud::Química médica | es_ES |
dc.subject | MicroRNA | es_ES |
dc.subject | Target genes | es_ES |
dc.subject | Long non-coding RNAs | es_ES |
dc.subject | Metabolic diseases | es_ES |
dc.subject | Bioinformatics analysis | es_ES |
dc.title | Crosstalk between microRNAs, the putative target genes and the lncRNA network in metabolic diseases | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.description.note | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) License. | es_ES |
dc.identifier.doi | 10.3892/mmr.2019.10595 | - |
dadun.citation.endingPage | 3554 | es_ES |
dadun.citation.number | 4 | es_ES |
dadun.citation.publicationName | Molecular Medicine Reports | es_ES |
dadun.citation.startingPage | 3543 | es_ES |
dadun.citation.volume | 20 | es_ES |
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