ArticleMolecular therapy. Nucleic acids2019
AntagomiR-103 and -107 Treatment Affects Cardiac Function and Metabolism.
Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed.
- Integrative transcriptomic and single-cell analysis reveals mitochondrial-related gene biomarkers in heart failure with preserved ejection fraction.Scientific reports · 2025Article
- miR-634 Mediated Aquaporin 5 Expression Regulates the Inflammatory Response and Apoptosis in Lipopolysaccharide-Induced Human Nasal Epithelial Cells.Cell biochemistry and biophysics · 2025Article
- CircRNA-based AntimiR therapy: A novel approach to hypertension treatment.Non-coding RNA research · 2025Review
- Mitochondrial microRNAs: Key Drivers in Unraveling Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- MicroRNAs in diabetic macroangiopathy.Cardiovascular diabetology · 2024Review
- Spinning Disk Confocal Microscopy for Optimized and Quantified Live Imaging of 3D Mitochondrial Network.International journal of molecular sciences · 2024Article
- Cardiac microRNAs: diagnostic and therapeutic potential.Archives of medical science : AMS · 2023Article
- Mitochondrial-related microRNAs and their roles in cellular senescence.Frontiers in physiology · 2023Review
- Cardiac Metabolism and MiRNA Interference.International journal of molecular sciences · 2022Review
- Systems Biology in Chronic Heart Failure-Identification of Potential miRNA Regulators.International journal of molecular sciences · 2022Article
- Review
- Circ-LTBP1 is involved in doxorubicin-induced intracellular toxicity in cardiomyocytes via miR-107/ADCY1 signal.Molecular and cellular biochemistry · 2022Article
- Overexpression of cytosolic long noncoding RNA cytb protects against pressure-overload-induced heart failure via sponging microRNA-103-3p.Molecular therapy. Nucleic acids · 2022Article
- microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis.Cell death discovery · 2022Article
- Isoflurane and low-level carbon monoxide exposures increase expression of pro-survival miRNA in neonatal mouse heart.Cell stress & chaperones · 2021Article
- A narrative review of the roles of the miR-15/107 family in heart disease: lessons and prospects for heart disease.Annals of translational medicine · 2021Review
- The Overexpression of NMHC IIA Promoted Invasion and Metastasis of Nasopharyngeal Carcinoma Cells.Journal of Cancer · 2021Article
- MicroRNAs as Potential Orchestrators of Alzheimer's Disease-Related Pathologies: Insights on Current Status and Future Possibilities.Frontiers in aging neuroscience · 2021Review
- Review
- Article
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-103/107 regulate systemic glucose metabolism and insulin sensitivity. For this reason, inhibitory strategies for these microRNAs are currently being tested in clinical trials. Given the high metabolic demands of the heart and the abundant cardiac expression of miR-103/107, we questioned whether antagomiR-mediated inhibition of miR-103/107 in C57BL/6J mice impacts on cardiac function. Notably, fractional shortening decreased after 6 weeks of antagomiR-103 and -107 treatment. This was paralleled by a prolonged systolic radial and circumferential time to peak and by a decreased global strain rate. Histology and electron microscopy showed reduced cardiomyocyte area and decreased mitochondrial volume and mitochondrial cristae density following antagomiR-103 and -107. In line, antagomiR-103 and -107 treatment decreased mitochondrial OXPHOS complexes' protein levels compared to scrambled, as assessed by mass spectrometry-based label-free quantitative proteomics. MiR-103/107 inhibition in primary cardiomyocytes did not affect glycolysis rates, but it decreased mitochondrial reserve capacity, reduced mitochondrial membrane potential, and altered mitochondrial network morphology, as assessed by live-cell imaging. Our data indicate that antagomiR-103 and -107 decrease cardiac function, cardiomyocyte size, and mitochondrial oxidative capacity in the absence of pathological stimuli. These data raise concern about the possible cardiac implications of the systemic use of antagomiR-103 and -107 in the clinical setting, and careful cardiac phenotyping within ongoing trials is highly recommended.
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Registered trials
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