Connexin43 cardiac gap junction remodeling: lessons from genetically engineered murine models.
Sudden cardiac death is responsible for several hundred thousand deaths each year in the United States. Multiple lines of evidence suggest that perturbation of gap junction expression and function in the heart, or what has come to be known as cardiac gap junction remodeling, plays a key mechanistic role in the pathophysiology of clinically significant cardiac arrhythmias. Here we review recent studies from our laboratory using genetically engineered murine models to explore mechanisms implicated in pathologic gap junction remodeling and their proarrhythmic consequences, with a particular focus on aberrant posttranslational phosphorylation of connexin43.
Leon H. Charney Division of Cardiology, New York University School of Medicine, 522 First Avenue, Smilow 801, New York, NY 10016, USA.
Benjamin F
BF
Remo
Steven
S
Giovannone
Glenn I
GI
Fishman
D000818:Animals; D030801:Animals, Genetically Modified; D001145:Arrhythmias, Cardiac / Q000378:metabolism; D018031:Connexin 43 / Q000378:metabolism*; D017629:Gap Junctions / Q000378:metabolism*; D006801:Humans; D051379:Mice; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational
D018031:Connexin 43