Abstract
Atrial myocyte (AM) is characterized by sparse transverse tubule invaginations and slow intracellular Ca2+ propagation but exhibits rapid contractile activation that is susceptible to loss of function during remodeling. Brandenburg et al (J Clin Invest 2016;126:3999, PMID 27643434) identified a membrane structure and Ca2+-signaling complex that may enhance the speed of atrial contraction independent of phospholamban regulation. This axial couplon is composed of voluminous axial tubules (ATs) with junctions to the sarcoplasmic reticulum (SR) and ryanodine receptor 2 (RyR2) clusters. In mouse AM, AT structures triggered Ca2+ release from the SR approximately 2 times faster at the AM center than at the surface. This release was with highly phosphorylated RyR2 clusters. In contrast, mice expressing phosphorylation-incompetent RyR2 displayed depressed AM sarcomere shortening and reduced contractile function. Atrial hypertrophy led to AT proliferation, with an increase in the high RyR2-pS2808 cluster fraction, thereby maintaining cytosolic Ca2+ signaling despite decreases in RyR2 cluster density. These authors conclude that AT couplon “super-hubs” thus underlie faster excitation-contraction coupling in health as well as hypertrophic compensatory adaptation.
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