| Literature DB >> 26391345 |
Kai-Chien Yang1, Jeanne M Nerbonne2.
Abstract
In the mammalian heart, multiple types of K(+) channels contribute to the control of cardiac electrical and mechanical functioning through the regulation of resting membrane potentials, action potential waveforms and refractoriness. There are similarly vast arrays of K(+) channel pore-forming and accessory subunits that contribute to the generation of functional myocardial K(+) channel diversity. Maladaptive remodeling of K(+) channels associated with cardiac and systemic diseases results in impaired repolarization and increased propensity for arrhythmias. Here, we review the diverse transcriptional, post-transcriptional, post-translational, and epigenetic mechanisms contributing to regulating the expression, distribution, and remodeling of cardiac K(+) channels under physiological and pathological conditions.Entities:
Keywords: Arrhythmias; Cardiac hypertrophy; Diabetes; Heart failure; Long non-coding RNAs; MicroRNAs; Myocardial excitability; Transcription factors
Mesh:
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Year: 2015 PMID: 26391345 PMCID: PMC4715991 DOI: 10.1016/j.tcm.2015.07.002
Source DB: PubMed Journal: Trends Cardiovasc Med ISSN: 1050-1738 Impact factor: 6.677