MicroRNA Profiling of Atrial Fibrillation in Canines: MiR-206 Modulates Intrinsic Cardiac Autonomic Nerve Remodeling by Regulating SOD1

Zhang, Yujiao; Zheng, Shaohua; Geng, Yangyang; Xue, Jiao; Wang, Zhongsu; Xie, Xide; Wang, Jiangrong; Zhang, Shuyu; Hou, Yuemei

doi:10.1371/journal.pone.0122674

Cited by 68 publications

(46 citation statements)

References 44 publications

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“…Gene therapy of a canine model with a lentivirus containing miR-206 resulted in truncation of the atrial APD beyond what was seen with atrial tachypacing alone. Accordingly, treatment with a lentivirus containing the antagonist anti-miR-206 resulted in AERP prolongation and reduced inducibility of AF (47). …”

Section: Targets For Gene Therapymentioning

confidence: 99%

Improving Atrial Fibrillation Therapy

Hucker

Hanley

Ellinor

2017

Journal of the American College of Cardiology

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Atrial fibrillation (AF) is an all-too-common and often challenging reality of clinical care. AF leads to significant morbidity and mortality; however, currently available treatments for AF have modest efficacy and high recurrence rates. In recent years, genetic therapy approaches have been explored in preclinical models of AF, and offer potential as a treatment modality with targeted delivery, tissue specificity, and therapy tailored to address mechanisms underlying the arrhythmia. However, many challenges remain before gene therapy can advance to a clinically relevant AF treatment. In this review, we will summarize the available published data on gene therapy and discuss the challenges, opportunities, and limitations of this approach.

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Section: Targets For Gene Therapymentioning

confidence: 99%

Improving Atrial Fibrillation Therapy

Hucker

Hanley

Ellinor

2017

Journal of the American College of Cardiology

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“…According to ZHANG et al (2015), microcfa-miR 206 is overexpressed 9.5 times more in dogs with AF when compared to dogs without arrhythmia. Expression of 16 other microRNAs is also dysregulated in dogs with AF.…”

Section: Arrhythmiasmentioning

confidence: 99%

“…MicroRNAs are potentially involved in a wide range of biological and pathological events. They are composed of approximately 19 to 25 nucleotides (ZHANG et al, 2015), transcribed from intranuclear DNA and transported to the cytoplasm, where a pre-microRNA is cleaved into mature microRNAs ( Figure 1) (CREEMERS et al, 2012). Increasingly, new evidence points to the role of microRNAs in the pathogenesis of several diseases.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs in veterinary cardiology

2017

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The use of biomarkers is an important recent development in veterinary medicine. Biomarkers allow non-invasive quantification of substances with diagnostic and prognostic potential in several diseases. The microRNAs are small, non-coding RNAs that regulate gene expression and are expressed in different forms in many diseases. Reduced or over-expression of microRNAs showed to be part of the pathogenesis of some heart diseases in humans and animals. Diagnostic and therapeutic value of measuring microRNAs in veterinary cardiology is increased because abnormal expression can be managed by the use of antagonists (in the case of overexpression) and mimicking (in the case of underexpression). Thus, this literature review aimed to compile scientific evidence of dysregulation of microRNAs expression in different cardiac diseases being one of the promises in the therapeutic field and diagnosis of veterinary cardiology. MicroRNAs not only have potential as a biomarker but may also help in elucidation of aspects of the pathogenesis of a variety of diseases.

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“…The authors found that KCNH2 transfer prolonged atrial action potential duration and prevented AF [9]. Similarly, Zhang's group found that miR-206 modulated intrinsic cardiac autonomic nerve remodeling in AF via right atrial tachypacing via the regulation of superoxide dismutase 1 (SOD1) in vivo, and this may be a potential therapeutic target for AF because it shortens the atrial effective refractory period [10]. Furthermore, many loci or target genes associated with ion channels, autonomic innervation, gap junctions, and substrate modifiers have been identified in preclinical studies to attenuate fibrosis, autonomic nerve sprouting, and AF duration [11][12][13].…”

Section: Introductionmentioning

confidence: 97%

“…That study underscores the fact that the pathogenesis of AF and its underlying molecular mechanisms are not completely understood. Recently, a series of preclinical studies suggested that genebased approaches could be used for the diagnosis and treatment of AF [9,10]. Most studies have had encouraging results that indicate the potential of gene-based therapies to combat AF.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Genes Involved in Persistent Atrial Fibrillation: Comparisons of ‘Trigger’ and ‘Substrate’ Differences

Zou

Yang

Shi

et al. 2018

Cell Physiol Biochem

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Background/Aims: Recent research has improved our understanding of the pulmonary vein and surrounding left atrial (LA-PV) junction and the left atrial appendage (LAA), which are considered the ‘trigger’ and ‘substrate’ in the development of atrial fibrillation (AF), respectively. Herein, with the aim of identifying the underlying potential genetic mechanisms, we compared differences in gene expression between LA-PV junction and LAA specimens via bioinformatic analysis. Methods: Microarray data of AF (GSE41177) were downloaded from the Gene Expression Omnibus database. In addition, linear models for microarray data limma powers differential expression analyses and weighted correlation network analysis (WGCNA) were applied. Results: From the differential expression analyses, 152 differentially expressed genes and hub genes, including LEP, FOS, EDN1, NMU, CALB2, TAC1, and PPBP, were identified. Our analysis revealed that the maps of extracellular matrix (ECM)-receptor interactions, PI3K-Akt and Wnt signaling pathways, and ventricular cardiac muscle tissue morphogenesis were significantly enriched. In addition, the WGCNA results showed high correlations between genes and related genetic clusters to external clinical characteristics. Maps of the ECM-receptor interactions, chemokine signaling pathways, and the cell cycle were significantly enriched in the genes of corresponding modules and closely associated with AF duration, left atrial diameter, and left ventricular ejection function, respectively. Similarly, mapping of the TNF signaling pathway indicated significant association with genetic traits of ischemic heart disease, hypertension, and diabetes comorbidity. Conclusions: The ECM-receptor interaction as a possible central node of comparison between LA-PV and LAA samples reflected the special functional roles of ‘triggers’ and ‘substrates’ and may be closely associated with AF duration. Furthermore, LEP, FOS, EDN1, NMU, CALB2, TAC1, and PPBP genes may be implicated in the occurrence and maintenance of AF through their interactions with each other.

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MicroRNA Profiling of Atrial Fibrillation in Canines: MiR-206 Modulates Intrinsic Cardiac Autonomic Nerve Remodeling by Regulating SOD1

Cited by 68 publications

References 44 publications

Improving Atrial Fibrillation Therapy

Improving Atrial Fibrillation Therapy

MicroRNAs in veterinary cardiology

Analysis of Genes Involved in Persistent Atrial Fibrillation: Comparisons of ‘Trigger’ and ‘Substrate’ Differences

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