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.
| Original language | English |
|---|---|
| Pages (from-to) | 209-218 |
| Number of pages | 10 |
| Journal | Trends in Cardiovascular Medicine |
| Volume | 26 |
| Issue number | 3 |
| DOIs | |
| State | Published - Apr 1 2016 |
Keywords
- Arrhythmias
- Cardiac hypertrophy
- Diabetes
- Heart failure
- Long non-coding RNAs
- MicroRNAs
- Myocardial excitability
- Transcription factors
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