ArticleBioMed research international2016
Role of miRNAs in Epicardial Adipose Tissue in CAD Patients with T2DM.
Article in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Epicardial adipose tissue mediates the association between circulating hsa-miR-4750-3p and coronary artery disease in patients with type 2 diabetes mellitus.Cardiovascular diabetology · 2026Observational
- Article
- Cardiovascular Dysfunction in Type 2 Diabetes: The Role of MicroRNAs.Handbook of experimental pharmacology · 2026Review
- Role of Human Epicardial Adipose Tissue-Derived miR-92a-3p in Myocardial Redox State.Journal of the American College of Cardiology · 2023Article
- The Role of Epicardial Adipose Tissue-Derived MicroRNAs in the Regulation of Cardiovascular Disease: A Narrative Review.Biology · 2023Review
- Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease.International journal of molecular sciences · 2022Article
- PDGF-BB promotes vascular smooth muscle cell migration by enhancing Pim-1 expression via inhibiting miR-214.Annals of translational medicine · 2021Article
- The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium.Frontiers in endocrinology · 2021Review
- Differential epigenetic factors in the prediction of cardiovascular risk in diabetic patients.European heart journal. Cardiovascular pharmacotherapy · 2020Review
- Integration of Gene Expression Profile Data of Human Epicardial Adipose Tissue from Coronary Artery Disease to Verification of Hub Genes and Pathways.BioMed research international · 2019Article
Corrections and comments
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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
Background. Epicardial adipose tissue (EAT) is identified as an atypical fat depot surrounding the heart with a putative role in the involvement of metabolic disorders, including obesity, type-2 diabetes mellitus, and atherosclerosis. We profiled miRNAs in EAT of metabolic patients with coronary artery disease (CAD) and type-2 diabetes mellitus (T2DM) versus metabolically healthy patients by microarray. Compared to metabolically healthy patients, we identified forty-two miRNAs that are differentially expressed in patients with CAD and T2DM from Xinjiang, China. Eleven miRNAs were selected as potential novel miRNAs according to P value and fold change. Then the potential novel miRNAs targeted genes were predicted via TargetScan, PicTar, and miRTarbase, and the function of the target genes was predicted via Gene Ontology (GO) analysis while the enriched KEGG pathway analyses of the miRNAs targeted genes were performed by bioinformatics software DAVID. Then protein-protein interaction networks of the targeted gene were conducted by online software STRING. Finally, using microarray, bioinformatics approaches revealed the possible molecular mechanisms pathogenesis of CAD and T2DM. A total of 11 differentially expressed miRNAs were identified and among them, hsa-miR-4687-3p drew specific attention. Bioinformatics analysis revealed that insulin signaling pathway is the central way involved in the progression of metabolic disorders. Conclusions. The current findings support the fact that miRNAs are involved in the pathogenesis of metabolic disorders in EAT of CAD patients with T2DM, and validation of the results of these miRNAs by independent and prospective study is certainly warranted.
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