Cardiac gap junctions are specialized membrane structures comprised of arrays of intercellular channels responsible for propagation of the cardiac impulse. These channels are formed by oligomerization of individual protein subunits known as connexins. In response to a broad array of pathologic stressors, gap junction expression is disturbed, resulting in aberrant cardiac conduction and increased propensity for rhythm disturbances. In this article, we review some of the recently identified molecular regulators of connexin assembly, membrane targeting, and degradation, focusing on the role of post-translational phosphorylation of connexin 43, the major gap junctional protein expressed in ventricular myocardium. We also describe efforts to engineer "designer" gap junctions that are resistant to pathologic remodeling.
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