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c-Jun N-terminal kinase activation contributes to reduced connexin43 and development of atrial arrhythmias

Jiajie Yan1, Wei Kong, Qiang Zhang

  • 1Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.

Cardiovascular Research
|December 18, 2012
PubMed

Insights

c-Jun N-terminal kinase (JNK) activation contributes to reduced connexin43 (Cx43) levels, promoting atrial fibrillation (AF). Targeting JNK may offer a new therapeutic strategy for AF prevention and treatment.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Electrophysiology

Background:

  • c-Jun N-terminal kinase (JNK) activation is linked to cardiovascular diseases and aging, conditions associated with increased atrial fibrillation (AF) risk.
  • The specific role of JNK in the development of AF, particularly its impact on gap junction proteins, remains largely unknown.

Purpose of the Study:

  • To investigate the contribution of JNK to the remodeling of gap junction connexin43 (Cx43).
  • To determine the role of JNK in the development of atrial fibrillation (AF).

Main Methods:

  • Experiments were conducted on young and aged rabbit atria and HL-1 atrial cells.
  • Assays included pacing-induced arrhythmias, optical mapping, biochemical analysis, JNK activation/inhibition, and Cx43 manipulation.

Main Results:

  • Aged atria exhibited increased arrhythmias, slower conduction velocity, elevated JNK activation, and reduced Cx43 compared to young atria.
  • JNK activation mimicked aged atrial phenotypes, causing Cx43 reduction, slower conduction, and irregular activity, effects reversed by JNK inhibition or Cx43 overexpression.

Conclusions:

  • JNK activation directly contributes to Cx43 reduction, a key mechanism promoting AF development.
  • Modulating JNK activity presents a potential novel therapeutic avenue for preventing and treating AF.
Abstract

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