Cardiac gap junctions and connexins: their role in atrial fibrillation and potential as therapeutic targets.
In the heart, changes in velocity and in patterns of conduction of myocardial electrical activity can affect cardiac rhythm and the coordination of contraction. Abnormal electrical coupling between cardiomyocytes through gap junctions is, therefore, considered an important factor in various pathophysiologic conditions. In the present report we summarize the literature on gap junctions and their structural proteins, the connexins, in the normal and fibrillating atrium. Putative implications of the recently reported remodelling of atrial gap junctions for stability of the arrhythmia will be discussed. Also the reversibility of the remodelling process will be addressed in the light of a potentially new therapeutic target for controlling the progression of atrial fibrillation (AF).
van der Velden
Huub M W
HM
Department of Medical Physiology, University Medical Centre Utrecht, Universiteitsweg 100, P.O. Box 85060, 3508 AB Utrecht, The Netherlands. velden@med.uu.nl
Jongsma
Habo J
HJ
D000818:Animals; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D002154:Calpain / Q000037:antagonists & inhibitors; D002908:Chronic Disease; D017630:Connexins / Q000378:metabolism*; D004594:Electrophysiology; D017629:Gap Junctions / Q000378:metabolism*; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology; D006801:Humans; D009206:Myocardium / Q000378:metabolism*
D017630:Connexins; D002154:Calpain