Fig. 7: Work model.

Under the action of β1-AA, the sustained activation of β1-AR is due to the decrease of endocytosis. Biased activation of β2-AR/Gi/GRK2 signaling pathway can promote the endocytosis of β1-AR that restricted by β1-AA, leading to the termination of β1-AA-induced continuous activation of β1-AR and improvement of cardiac structure and function.