ArticlePloS one2015
MicroRNA profiling of atrial fibrillation in canines: miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- MicroRNAs in Atrial Fibrillation: from Expression Signatures to Functional Implications.Cardiovascular drugs and therapy · 2017Pooled it
- Identification of altered salivary microRNAs in Cavalier King Charles Spaniels affected by mitral valve disease at different ACVIM stages.Scientific reports · 2026Article
- Gene Therapies in Atrial Fibrillation.Journal of cardiovascular translational research · 2025Review
- Autonomic dysregulation and atrial arrhythmias.American journal of physiology. Cell physiology · 2025Review
- Epigenetic Drivers of Atrial Fibrillation: Mechanisms, Biomarkers, and Therapeutic Targets.International journal of molecular sciences · 2025Review
- MicroRNAs in atrial fibrillation - have we discovered the Holy Grail or opened a Pandora's box?Frontiers in pharmacology · 2025Review
- Metabolomics in Atrial Fibrillation: Unlocking Novel Biomarkers and Pathways for Diagnosis, Prognosis, and Personalized Treatment.Journal of clinical medicine · 2024Review
- Gene therapy for atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Identification of Plasmatic MicroRNA-206 as New Predictor of Early Recurrence of Atrial Fibrillation After Catheter Ablation Using Next-generation Sequencing.Molecular diagnosis & therapy · 2024Article
- MicroRNAs in Atrial Fibrillation: Mechanisms, Vascular Implications, and Therapeutic Potential.Biomedicines · 2024Review
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Assessing the use of blood microRNA expression patterns for predictive diagnosis of myxomatous mitral valve disease in dogs.Frontiers in veterinary science · 2024Article
- Tic-Tac: A Translational Approach in Mechanisms Associated with Irregular Heartbeat and Sinus Rhythm Restoration in Atrial Fibrillation Patients.International journal of molecular sciences · 2023Review
- Altered MicroRNA Maturation in Ischemic Hearts: Implication of Hypoxia on XPO5 and DICER1 Dysregulation and RedoximiR State.Antioxidants (Basel, Switzerland) · 2023Article
- Non-coding RNAs in human health and disease: potential function as biomarkers and therapeutic targets.Functional & integrative genomics · 2023Review
- Genome Editing and Atrial Fibrillation.Advances in experimental medicine and biology · 2023Article
- A review on microRNA detection and expression studies in dogs.Frontiers in veterinary science · 2023Review
- Research progress of non-coding RNA in atrial fibrillation.Frontiers in cardiovascular medicine · 2023Review
- Emerging Roles of Micrornas in Veterinary Cardiology.Veterinary sciences · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA critical mechanism in atrial fibrillation (AF) is cardiac autonomic nerve remodeling (ANR). MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level. Numerous miRNAs are involved in diseases of the nervous and cardiovascular systems.
objectiveWe aimed to assess the underlying role of miRNAs in regulating cardiac ANR in AF by right atrial tachypacing (A-TP) in canines. METHODS AND
resultsFollowing 4-week A-TP, the superior left ganglionated plexuses (SLGPs), which are embedded in the fat pads of the left atrium, were subjected to miRNA expression profiling to screen preferentially expressed miRNAs. Sixteen miRNAs showed significantly differential expression between the control and A-TP groups, including miR-206, miR-203, miR-224 and miR-137. In particular, we focused on miR-206, which was elevated ~10-fold in A-TP dogs. Forced expression of miR-206 through lentiviral infection based on A-TP in vivo significantly shortened the atrial effective refractory period (AERP) (81 ± 7 vs. 98 ± 7 ms, P < 0.05). Immunohistochemical analysis showed that the regeneration of nerves increased more than 2-fold by miR-206 overexpression (P < 0.01). The expression of superoxide dismutase 1 (SOD1) was repressed by miR-206 overexpression by Western blot and luciferase assay, indicative of SOD1 as a direct target of miR-206. Overexpression of miR-206 increased reactive oxygen species (ROS) levels in vitro and in vivo, whereas miR-206 silencing attenuated irradiation- or A-TP-induced ROS. Knockdown of SOD1 effectively abolished ROS reduction caused by miR-206 silencing.
conclusionsOur results found the differential expression of miRNAs in response to ANR in AF and elucidated the important role of miR-206 by targeting SOD1. The study illustrated the novel molecular mechanism of ANR and indicated a potential therapeutic target for AF.
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