Electrical heart disease: Genetic and molecular basis of cardiac arrhythmias in normal structural hearts

Farwell, David; Gollob, Michael H.

doi:10.1016/s0828-282x(07)71001-2

Cited by 24 publications

(15 citation statements)

References 72 publications

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“…7,28 In humans, the relationship among genetics, arrhythmias, and sudden death is also under investigation. [14][15][16][17][18] Our division of the overall disease trait into multiple traits was supported by the observed differences in heritability estimates and ages of onset and the fairly low estimates of genetic correlation among the 3 traits.…”

Section: Pattern Of Inheritance: Dependence On Correct Phenotype Idenmentioning

confidence: 89%

“…In people, important advances have been made in the understanding of the genetic basis of inherited arrhythmic disorders with loss of repolarization reserve including the long QT syndromes, [9][10][11][12] Brugada syndrome, 13 and others. [14][15][16][17][18][19] Causative mutations have primarily been identified in genes encoding specific sodium and potassium channel proteins involved in repolarization. [9][10][11][12][13][14][15][16][17][18][19] In affected GSDs, abnormalities of ion current densities of potassium channels and calcium cycling indicate a global disruption of repolarization reserve.…”

mentioning

confidence: 99%

“…[14][15][16][17][18][19] Causative mutations have primarily been identified in genes encoding specific sodium and potassium channel proteins involved in repolarization. [9][10][11][12][13][14][15][16][17][18][19] In affected GSDs, abnormalities of ion current densities of potassium channels and calcium cycling indicate a global disruption of repolarization reserve. [20][21][22][23][24][25][26][27][28][29][30] Futhermore, heterogeneous sympathetic innervation has been identified.…”

mentioning

confidence: 99%

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Genetic Analysis of Ventricular Arrhythmia in Young German Shepherd Dogs

Cruickshank

Quaas

et al. 2009

Veterinary Internal Medicne

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Section: Pattern Of Inheritance: Dependence On Correct Phenotype Idenmentioning

confidence: 89%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Genetic Analysis of Ventricular Arrhythmia in Young German Shepherd Dogs

Cruickshank

Quaas

et al. 2009

Veterinary Internal Medicne

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“…There are multiple genetically determined cardiac pathologies, with or without accompanying structural cardiopathy, that may predispose to the appearance of arrhythmias and sudden death [29][30][31] . These diseases are the product of alterations in the genetic encoding of four large families of proteins:…”

Section: Genetics and Sudden Death In Athletesmentioning

confidence: 99%

Genetics and Sports

2009

Medicine and Sport Science

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There have been great scientific and technical advances in biomedicine in the last few years, particularly after the description of the human genome. These improvements have gradually been applied in diverse fields that have gone beyond the study of the disease to enter the study of health. The latter includes research in the field of physical and sports activity. Genetics therefore provides the scientific knowledge that helps us to optimise the performance of high level sportsmen/women, to reap the benefits of carrying out physical exercise and/or to perform a safe sports practice by evaluating the risk of a hereditary disease associated to sudden death in sportsmen/women.

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“…Genetic and epigenetic alterations have been linked to arrhythmias. [12][13][14][15] Now, it is being recognized that defects of messenger RNA (mRNA) processing can cause arrhythmogenesis ( Table 1). This review focuses on mRNA processing, especially pre-mRNA splicing and mRNA stability and its impact on cardiac arrhythmias.…”

Section: Introductionmentioning

confidence: 99%

Ion channel messenger RNA processing defects and arrhythmia

Zhou¹,

Dudley²

2014

CBF

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Messenger RNA (mRNA) processing is an essential step for the expression of most eukaryote genes. Ion channels are critical for proper electrical activity in the heart, and perturbations of these channels are known to cause arrhythmia. Recently, mRNA processing defects have been shown to contribute to altered ion channel activity and arrhythmogenesis. Abnormal pre-mRNA splicing of cardiac ion channels, including the cardiac sodium channel, potassium channels, and calcium channels, because of mutations of the cis-elements within the RNA or abnormal expression of splicing factors, has been documented to contribute to arrhythmic risk. In addition to pre-mRNA splicing, other mRNA processing events, such as 3′-end formation and mRNA turnover, are also disrupted in cardiac diseases, such as congenital heart disease caused by mutation at the 3′-untranslated region of GATA4. mRNA stability is also dysregulated by altered expression of microRNAs in atrial fibrillation. In this review, we discuss our current understanding of how mRNA processing defects contribute to the risk of arrhythmias and how monitoring the products of abnormal processing may lead to diagnostic tests for arrhythmic risk.

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Electrical heart disease: Genetic and molecular basis of cardiac arrhythmias in normal structural hearts

Cited by 24 publications

References 72 publications

Genetic Analysis of Ventricular Arrhythmia in Young German Shepherd Dogs

Genetic Analysis of Ventricular Arrhythmia in Young German Shepherd Dogs

Genetics and Sports

Ion channel messenger RNA processing defects and arrhythmia

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