The present study was undertaken in an attempt to assess whether autophagic flux is entirely activated in synthesis or impaired in degradative stage during clinical and experimental AF, whether autophagy is implicated in atrial electrical remodeling, and whether a synergic role for autophagy and UPS triggers the selective degradation of Cav1.2 in atrial myocytes to promote AF. Here, CACNA1C is linked to atrial fibrillation.