ADRB1 and familial dilated cardiomyopathy: Persistent receptor stimulation induces excessive activation of the cAMP signaling pathway, calcium overload, and mitochondrial dysfunction, ultimately leading to cardiomyocyte apoptosis and ventricular remodeling.[11] Iwata et al demonstrated that anti-β1-AR antibody levels are markedly elevated in patients with DCM and significantly correlate with the degree of left ventricular systolic impairment.[12] Furthermore, removal of these antibodies via immunoadsorption has been associated with improvements in left ventricular ejection fraction (LVEF), suggesting a potential pathogenic role.