Disruption of caveolae in sinoatrial node leads to sinoatrial node dysfunction, revealing caveolar signaling as crucial for stable pacemaking and a therapeutic target.
Caveolar compartmentalization is essential for stable sinoatrial rhythmicity, and its disruption in heart failure leads to sinoatrial node dysfunction, representing a novel therapeutic target.
SAN pacemaking is driven by complex protein interactions within a nanoscale caveolar pacemaker signalosome. Disruption of caveolae leads to SND, demonstrating a new dimension of SAN remodeling and revealing a novel therapeutic target.
Lang et al. (2026) studied this question. Disruption of caveolae in sinoatrial node leads to sinoatrial node dysfunction, revealing caveolar signaling as crucial for stable pacemaking and a therapeutic target.