title: Gene therapies for arrhythmias in heart failure.
abstract: In this article, we review recent advances in our understanding of arrhythmia mechanisms in the failing heart. We focus on changes in repolarization, conduction, and intracellular calcium cycling because of their importance to the vast majority of clinical arrhythmias in heart failure. We highlight recent efforts to combat arrhythmias using gene-based approaches that target ion channel, gap junction, and calcium cycling proteins. We further discuss the advantages and limitations associated with individual approaches.
authors.affiliation: The Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA, fadi.akar@mssm.edu.
authors.forename: Fadi G
authors.initials: FG
authors.lastname: Akar
authors.forename: Roger J
authors.initials: RJ
authors.lastname: Hajjar
mesh_terms: D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000235:genetics* / Q000503:physiopathology / Q000628:therapy; D020013:Calcium Signaling; D018031:Connexin 43 / Q000235:genetics / Q000378:metabolism; D015316:Genetic Therapy; D006333:Heart Failure / Q000235:genetics* / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D007473:Ion Channels / Q000235:genetics* / Q000378:metabolism
chemical_list: D018031:Connexin 43; D007473:Ion Channels