A leaky voltage sensor domain of cardiac sodium channels causes arrhythmias associated with dilated cardiomyopathy

Moreau, Adrien; Gosselin-Badaroudine, Pascal; Mercier, Aurélie; Burger, Bettina; Keller, Dagmar I.; Chahine, Mohamed

doi:10.1038/s41598-018-31772-0

Cited by 30 publications

(21 citation statements)

References 56 publications

(55 reference statements)

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“…These, in turn, lead to abnormal contraction and relaxation or dysregulated ion transportation across cell membranes. As a structural heart disease, DCM causes the dilatation of the heart ventricle and the damage of systolic function, leading to heart failure as the final stage [ 22 ]. Despite some progress in the treatment and diagnosis, the prognosis of DCM patients remains poor at the current stage.…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Hub Genes and miRNAs in Dilated Cardiomyopathy

Huang

Wen

Wang

et al. 2020

BioMed Research International

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Purpose. The aim of this study is to identify hub genes and miRNAs by the miRNA-mRNA interaction network in dilated cardiomyopathy (DCM) disease. Methods. The differentially expressed miRNAs (DEMis) and mRNAs (DEMs) were selected using data of DCM patients downloaded from the GEO database (GSE112556 and GSE3585). Gene Ontology (GO) pathway analysis and transcription factor enrichment analysis were used for selecting DEMis, and the target mRNAs of DEMis were filtered by using miRDB, miRTarBase, and TargetScan. Cytoscape software was used to visualize the network between miRNAs and mRNAs and calculate the hub genes. GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were used to analyze the mRNAs in the regulatory network. Results. A total of 9 DEMis and 281 DEMs were selected, from which we reconstructed the miRNA-mRNA network consisting of 7 miRNAs and 51 mRNAs. The top 10 nodes, miR-144-3p, miR-363-3p, miR-9-3p, miR-21-3p, miR-144-5p, miR-338-3p, ID4 (inhibitor of DNA binding/differentiation 4), miR-770-5p, PIK3R1 (p85α regulatory subunit of phosphoinositide 3-kinase (PI3K)), and FN1 (fibronectin 1), were identified as important regulators. Conclusions. The study uncovered several important hub genes and miRNAs involved in the pathogenesis of DCM, among which, the miR-144-3p/FN1 and miR-9-3p/FN1 pathways may play an important role in myocardial fibrosis, which can help identify the etiology of DCM, and provide potential therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Hub Genes and miRNAs in Dilated Cardiomyopathy

Huang

Wen

Wang

et al. 2020

BioMed Research International

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“…Genes such as LGALS3, FKBP5, and SCN5A are essential in determining not only the severity of heart disease, but also the prevalence of heart disease 6,24,25 . SCN5A is key in encoding for sodium, specifically for the cardiac sodium channel 26 . The SCN5A gene specifically instigates and transmits action potentials, this correlates to deciding the cardiac impulses and conduction 27 .…”

Section: How Genetics Contributes To Heart Disease In African-americansmentioning

confidence: 99%

Causes for increased incidence of heart disease Among African American Community

Chandra¹,

Sharpe²

2020

Arşiv Kaynak Tarama Dergisi

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Cardiovascular disease is a worldwide phenomenon. While it is found in men and women almost equally, it is found in almost disproportionately high rates in African-Americans. African-Americans compromise a smaller portion of the population yet, they have higher risk of suffering from heart disease than most minority groups. The increased probability of suffering for heart disease is based on commonly known factors such as stress, lifestyle choice, and biochemistry levels. But the possibility of developing cardiovascular disease also relies on less thought of factors such as direct environment, socioeconomic status, and even perceived racism. This review sought to understand why African-Americans have such a high prevalence of heart disease, and even heart attack and death. We hope that in the future researchers can find more effective ways to minimize both traditional and non-traditional risk factors, which cause elevated frequency of heart disease in African-Americans. By minimizing the risk factors, improvements can be made to overall health and hopefully decreased incidence of heart disease.

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“…Mutations in non-sarcomeric cardiomyopathy genes, such those involved with ion channels, metabolic function, and growth pathways, are outside the scope of this review, but these too have been profitably studied in iPSC systems (Moretti et al 2010;Cashman et al 2016;Hinson et al 2016;Joanne et al 2016;Josowitz et al 2016;Judge et al 2017;Lee et al 2017;Liu et al 2017;Lu et al 2017;Ben Jehuda et al 2018;Hallas et al 2018;Moreau et al 2018;Zhan et al 2018;Li et al 2018b).…”

Section: Ipsc-derived Cardiomyocytesmentioning

confidence: 99%

Modelling sarcomeric cardiomyopathies with human cardiomyocytes derived from induced pluripotent stem cells

Sewanan

2019

The Journal of Physiology

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Cardiomyocytes derived from human induced pluripotent stem cells (iPSCs) provide a unique opportunity to understand the pathophysiological effects of genetic cardiomyopathy mutations. In particular, these cells hold the potential to unmask the effects of mutations on contractile behaviour in vitro, providing new insights into genotype-phenotype relationships. With this goal in mind, several groups have established iPSC lines that contain sarcomeric gene Lorenzo Rakesh Sewanan is an MD-PhD candidate in the Department of Biomedical Engineering at Yale University. His current research interests lie at the intersection of cardiac tissue engineering, biomechanics, and mechanobiology, with particular application to understanding mechanisms underlying cardiomyopathy and heart failure. He hopes to pursue a career as an academic cardiologist and a physician-scientist with a continued emphasis on the role of mechanics and mechanobiology in cardiac health and disease. Stuart Campbell is an Associate Professor of Biomedical Engineering at Yale University. His laboratory is focused on studying the biophysical mechanisms underlying inherited cardiomyopathies. His approach combines new computational models of muscle function and engineered heart tissue constructs made from human induced pluripotent stem cells. He holds degrees in bioengineering from Washington State University (BS, 2004) and the

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A leaky voltage sensor domain of cardiac sodium channels causes arrhythmias associated with dilated cardiomyopathy

Cited by 30 publications

References 56 publications

Integrated Analysis of Hub Genes and miRNAs in Dilated Cardiomyopathy

Integrated Analysis of Hub Genes and miRNAs in Dilated Cardiomyopathy

Causes for increased incidence of heart disease Among African American Community

Modelling sarcomeric cardiomyopathies with human cardiomyocytes derived from induced pluripotent stem cells

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