Age-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations.

ABSTRACT: Understanding the cellular-molecular substrates of heart disease is key to the development of cardiac specific therapies and to the prevention of off-target effects by non-cardiac targeted drugs. One of the primary targets for therapeutic intervention has been the human ether a go-go (hERG) K+ channel that, together with the KCNQ channel, controls the rate and efficiency of repolarization in human myocardial cells. Neither of these channels plays a major role in adult mouse heart function; however, we show here that the hERG homolog seizure (sei), along with KCNQ, both contribute significantly to adult heart function as they do in humans. In Drosophila, mutations in or cardiac knockdown of sei channels cause arrhythmias that become progressively more severe with age. Intracellular recordin

SUBMITTER: Ocorr K 

PROVIDER: S-EPMC5459509 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature