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 languageEnglish
Pages (from-to)209-218
Number of pages10
JournalTrends in Cardiovascular Medicine
Issue number3
StatePublished - Apr 1 2016


  • Arrhythmias
  • Cardiac hypertrophy
  • Diabetes
  • Heart failure
  • Long non-coding RNAs
  • MicroRNAs
  • Myocardial excitability
  • Transcription factors


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