Gene therapy for inherited arrhythmias

Standard

Gene therapy for inherited arrhythmias. / Bezzerides, Vassilios J; Prondzynski, Maksymilian; Carrier, Lucie; Pu, William T.

in: CARDIOVASC RES, Jahrgang 116, Nr. 9, 15.07.2020, S. 1635-1650.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ReviewForschung

Harvard

Bezzerides, VJ, Prondzynski, M, Carrier, L & Pu, WT 2020, 'Gene therapy for inherited arrhythmias', CARDIOVASC RES, Jg. 116, Nr. 9, S. 1635-1650. https://doi.org/10.1093/cvr/cvaa107

APA

Bezzerides, V. J., Prondzynski, M., Carrier, L., & Pu, W. T. (2020). Gene therapy for inherited arrhythmias. CARDIOVASC RES, 116(9), 1635-1650. https://doi.org/10.1093/cvr/cvaa107

Vancouver

Bezzerides VJ, Prondzynski M, Carrier L, Pu WT. Gene therapy for inherited arrhythmias. CARDIOVASC RES. 2020 Jul 15;116(9):1635-1650. https://doi.org/10.1093/cvr/cvaa107

Bibtex

@article{e72428c06b0c410fb8f7aee3b961c8fb,
title = "Gene therapy for inherited arrhythmias",
abstract = "Inherited arrhythmias are disorders caused by one or more genetic mutations that increase the risk of arrhythmia, which result in life-long risk of sudden death. These mutations either primarily perturb electrophysiological homeostasis (e.g. long QT syndrome and catecholaminergic polymorphic ventricular tachycardia), cause structural disease that is closely associated with severe arrhythmias (e.g. hypertrophic cardiomyopathy), or cause a high propensity for arrhythmia in combination with altered myocardial structure and function (e.g. arrhythmogenic cardiomyopathy). Currently available therapies offer incomplete protection from arrhythmia and fail to alter disease progression. Recent studies suggest that gene therapies may provide potent, molecularly targeted options for at least a subset of inherited arrhythmias. Here, we provide an overview of gene therapy strategies, and review recent studies on gene therapies for catecholaminergic polymorphic ventricular tachycardia and hypertrophic cardiomyopathy caused by MYBPC3 mutations.",
author = "Bezzerides, {Vassilios J} and Maksymilian Prondzynski and Lucie Carrier and Pu, {William T}",
note = "Published on behalf of the European Society of Cardiology. All rights reserved. {\textcopyright} The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.",
year = "2020",
month = jul,
day = "15",
doi = "10.1093/cvr/cvaa107",
language = "English",
volume = "116",
pages = "1635--1650",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "9",

}

RIS

TY - JOUR

T1 - Gene therapy for inherited arrhythmias

AU - Bezzerides, Vassilios J

AU - Prondzynski, Maksymilian

AU - Carrier, Lucie

AU - Pu, William T

N1 - Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.

PY - 2020/7/15

Y1 - 2020/7/15

N2 - Inherited arrhythmias are disorders caused by one or more genetic mutations that increase the risk of arrhythmia, which result in life-long risk of sudden death. These mutations either primarily perturb electrophysiological homeostasis (e.g. long QT syndrome and catecholaminergic polymorphic ventricular tachycardia), cause structural disease that is closely associated with severe arrhythmias (e.g. hypertrophic cardiomyopathy), or cause a high propensity for arrhythmia in combination with altered myocardial structure and function (e.g. arrhythmogenic cardiomyopathy). Currently available therapies offer incomplete protection from arrhythmia and fail to alter disease progression. Recent studies suggest that gene therapies may provide potent, molecularly targeted options for at least a subset of inherited arrhythmias. Here, we provide an overview of gene therapy strategies, and review recent studies on gene therapies for catecholaminergic polymorphic ventricular tachycardia and hypertrophic cardiomyopathy caused by MYBPC3 mutations.

AB - Inherited arrhythmias are disorders caused by one or more genetic mutations that increase the risk of arrhythmia, which result in life-long risk of sudden death. These mutations either primarily perturb electrophysiological homeostasis (e.g. long QT syndrome and catecholaminergic polymorphic ventricular tachycardia), cause structural disease that is closely associated with severe arrhythmias (e.g. hypertrophic cardiomyopathy), or cause a high propensity for arrhythmia in combination with altered myocardial structure and function (e.g. arrhythmogenic cardiomyopathy). Currently available therapies offer incomplete protection from arrhythmia and fail to alter disease progression. Recent studies suggest that gene therapies may provide potent, molecularly targeted options for at least a subset of inherited arrhythmias. Here, we provide an overview of gene therapy strategies, and review recent studies on gene therapies for catecholaminergic polymorphic ventricular tachycardia and hypertrophic cardiomyopathy caused by MYBPC3 mutations.

U2 - 10.1093/cvr/cvaa107

DO - 10.1093/cvr/cvaa107

M3 - SCORING: Review article

C2 - 32321160

VL - 116

SP - 1635

EP - 1650

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 9

ER -