β2-Adrenergic receptor (β2AR) agonists are clinically used to elicit rapid bronchodilation for the treatment of bronchospasms in pulmonary diseases such as asthma and COPD, both of which exhibit characteristically high levels of reactive oxygen species (ROS); likely secondary to over-expression of ROS generating enzymes and chronically heightened inflammation. Interestingly, β2AR has long-been linked to ROS, yet the involvement of ROS in β2AR function has not been as vigorously studied as other aspects of β2AR signaling. Herein, we discuss the existing body of evidence linking β2AR activation to intracellular ROS generation and importantly, the role of ROS in regulating β2AR function. The reciprocal interplay of the β2AR and ROS appear to endow this receptor with the ability to self-regulate signaling efficacy and ligand binding, hereby unveiling a redox-axis that may be unfavorably altered in pathological states contributing to both disease progression and therapeutic drug responses.
Keywords: Cysteine-S-sulfenation; G protein-coupled receptors; Reactive oxygen species; Redox; β2AR.
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