Abstract

Spontaneous beating of sinoatrial node (SAN) cells is mediated by a complex coupled system of both membrane- and Ca2+-clocks. Distinct from ventricular myocytes, SAN myocytes typically lack transversal tubules but instead display rich caveolae, i.e., small Ω-shaped invaginations of the plasma membrane. Disruption of caveolae has been associated with dysregulation of caveolar-associated ion channels and transporters and linked to Long QT syndrome and heart failure. However, their functional role in SAN pacemaking remains to be elucidated mechanistically.

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