ArticleInternational journal of genomics2017
Overexpression of Chromosome 21 miRNAs May Affect Mitochondrial Function in the Hearts of Down Syndrome Fetuses.
Article in International journal of genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Dysregulated miR-155 and miR-125b Are Related to Impaired B-cell Responses in Down Syndrome.Frontiers in immunology · 2018Trial
- Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- Oxidative Stress and Down Syndrome: A Systematic Review.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?Aging and disease · 2025Review
- Gene Expression Studies in Down Syndrome: What Do They Tell Us about Disease Phenotypes?International journal of molecular sciences · 2024Review
- The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023Review
- Genetics and Molecular Basis of Congenital Heart Defects in Down Syndrome: Role of Extracellular Matrix Regulation.International journal of molecular sciences · 2023Review
- Profiling of circulating chromosome 21-encoded microRNAs, miR-155, and let-7c, in down syndrome.Molecular genetics & genomic medicine · 2022Article
- Future Perspectives in Oxidative Stress in Trisomy 13 and 18 Evaluation.Journal of clinical medicine · 2022Review
- Differential microRNA expression profile in blood of children with Down syndrome suggests a role in immunological dysfunction.Human cell · 2022Article
- Overexpression of the Hsa21 Transcription Factor RUNX1 Modulates the Extracellular Matrix in Trisomy 21 Cells.Frontiers in genetics · 2022Article
- Application of Induced Pluripotent Stem Cell-Derived Models for Investigating microRNA Regulation in Developmental Processes.Frontiers in genetics · 2022Review
- The Potential Role of miRNAs as Predictive Biomarkers in Neurodevelopmental Disorders.Journal of molecular neuroscience : MN · 2021Review
- Human Trisomic iPSCs from Down Syndrome Fibroblasts Manifest Mitochondrial Alterations Early during Neuronal Differentiation.Biology · 2021Article
- PPARγ/PGC1α signaling as a potential therapeutic target for mitochondrial biogenesis in neurodegenerative disorders.Pharmacology & therapeutics · 2021Review
- Targeting Mitochondrial Network Architecture in Down Syndrome and Aging.International journal of molecular sciences · 2020Review
- The Population Prevalence, Associations of Congenital Heart Defect and Mortality Risk for Down's Syndrome in South Korea Based on National Health Insurance Service (NHIS) Data.Clinical epidemiology · 2020Article
- Mature miR-99a Upregulation in the Amniotic Fluid Samples from Female Fetus Down Syndrome Pregnancies: A Pilot Study.Medicina (Kaunas, Lithuania) · 2019Article
- Pioglitazone Improves Mitochondrial Organization and Bioenergetics in Down Syndrome Cells.Frontiers in genetics · 2019Article
- Mitochondrial dysfunction in down syndrome: molecular mechanisms and therapeutic targets.Molecular medicine (Cambridge, Mass.) · 2018Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dosage-dependent upregulation of most of chromosome 21 (Hsa21) genes has been demonstrated in heart tissues of fetuses with Down syndrome (DS). Also miRNAs might play important roles in the cardiac phenotype as they are highly expressed in the heart and regulate cardiac development. Five Hsa21 miRNAs have been well studied in the past: miR-99a-5p, miR-125b-2-5p, let-7c-5p, miR-155-5p, and miR-802-5p but few information is available about their expression in trisomic tissues. In this study, we evaluated the expression of these miRNAs in heart tissues from DS fetuses, showing that miR-99a-5p, miR-155-5p, and let-7c-5p were overexpressed in trisomic hearts. To investigate their role, predicted targets were obtained from different databases and cross-validated using the gene expression profiling dataset we previously generated for fetal hearts. Eighty-five targets of let-7c-5p, 33 of miR-155-5p, and 10 of miR-99a-5p were expressed in fetal heart and downregulated in trisomic hearts. As nuclear encoded mitochondrial genes were found downregulated in trisomic hearts and mitochondrial dysfunction is a hallmark of DS phenotypes, we put special attention to let-7c-5p and miR-155-5p targets downregulated in DS fetal hearts and involved in mitochondrial function. The let-7c-5p predicted target
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Registered trials
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