IL10 and myocardial infarction: β2‐AR,[38] while another report has shown that β1‐AR blockade suppresses neutrophil activation thus reduces the brain‐damaging effects.[39] In acute phase of inflammation, β2‐AR acts as co‐activator to enhance TLR pathway's response to LPS in innate immune cells and promote IL‐10 autosecretion to further modulate the inflammatory response,[40] while during the long‐term reparative phase, chronic activation of β2‐AR on myeloid cells is implicated to fibrotic process following myocardial infarction (MI) with up‐regulation of Anax1.