Abstract
Every heartbeat is initiated by a spontaneous electrical signal generated inside the cardiac pacemaker. In mammals, including humans, aging leads to the slowdown of the pacemaker rate, which can lead to pathological dysfunction and death. However, the mechanisms behind the age-associated slowdown of the pacemaker are not well understood. The automaticity of the pacemaker relies on a finely tuned balance of ionic currents, where L-type calcium channels play a central role. CaV1.2 and CaV1.3 channels are key players involved in the diastolic depolarization phase and action potential upstroke.
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