β2-adrenergic receptor autoantibodies alleviated myocardial damage induced by β1-adrenergic receptor autoantibodies in heart failure

β2-AAs were capable of antagonizing the effects imposed by β1-AAs both in vitro and in vivo. The imbalance of β1-AAs and β2-AAs in patients with HF is a mechanism underlying HF progression, and the increasing ratio of β1-AAs/β2-AAs should be considered a clinical assessment factor for the deterioration of cardiac function in patients with HF.