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Atrial fibrillation in KCNE1-null mice.

Joel Temple1, Patricio Frias, Jeffrey Rottman

  • 1Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232-6602, USA.

Circulation Research
|June 11, 2005
PubMed
Summary

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Mice lacking the KCNE1 protein partner experienced spontaneous atrial fibrillation. This was linked to increased K+ currents, shortened atrial action potentials, and enhanced susceptibility, revealing new insights into cardiac arrhythmia mechanisms.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Electrophysiology

Background:

  • Atrial fibrillation (AF) is a common cardiac arrhythmia with poorly understood molecular underpinnings.
  • Mutations in KCNQ1, a component of cardiac potassium channels, are linked to familial AF, but in vivo mechanisms are unclear.

Purpose of the Study:

  • To investigate the in vivo role of KCNE1 in cardiac electrophysiology and atrial fibrillation.
  • To elucidate the molecular mechanisms by which KCNE1 deficiency affects atrial action potentials and arrhythmia susceptibility.

Main Methods:

  • Generation and analysis of KCNE1 knockout (KCNE1-/-) mice.
  • Electrophysiological recordings of atrial and ventricular action potentials.
  • Patch-clamp studies on atrial myocytes and heterologous expression systems (CHO cells) to assess ion channel function.

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Last Updated: Jun 28, 2026

Programmed Electrical Stimulation in Mice
07:29

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Published on: May 27, 2010

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Published on: March 12, 2013

Main Results:

  • KCNE1-/- mice exhibited spontaneous atrial fibrillation episodes without changes in atrial size or structure.
  • Atrial action potentials were unexpectedly shortened in KCNE1-/- mice, contrary to human ventricular findings.
  • Increased K+ currents, including those sensitive to chromanol 293B, were observed in KCNE1-/- atrial cells.
  • Rapid pacing revealed that KCNE1 modulates KCNQ1 channel kinetics, preventing current accumulation at high heart rates.

Conclusions:

  • KCNE1 deficiency in mice leads to increased atrial outward K+ currents and shortened atrial action potentials.
  • These electrophysiological changes enhance susceptibility to atrial fibrillation, highlighting KCNE1's critical role in maintaining cardiac rhythm.
  • The findings provide novel molecular insights into the pathogenesis of atrial fibrillation.