Formoterol Reduces the Pro-Inflammatory Phenotype by Enhancing the Activity of Glutaminase in Monocyte-Derived Macrophages in the CVB3-Induced Viral Myocarditis.

Background: Viral myocarditis (VMC) plays a significant role in heart failure, and there is currently a shortage of available targeted treatments. Macrophage phenotype and function are closely associated with the beta-2 adrenergic receptor (β2-AR).

Method: This research employed a BALB/c mouse model of VMC generated using Coxsackievirus B3 (CVB3), and the β2-AR agonist formoterol was administered as treatment.