The role of β₂-adrenergic receptors in ischemic stroke

Ischemic stroke is a common cerebrovascular disease with an increasing incidence year by year, and it remains one of the leading causes of death and disability worldwide. The β2-adrenergic receptor (β2-AR), a member of the G protein-coupled receptor (GPCR) family, functions on the cell membrane by binding to specific ligands such as epinephrine (E) and norepinephrine (NE), thereby regulating intracellular signal transduction. Recent studies have revealed that the β2-AR signaling pathway exerts multifaceted neuroprotective effects on ischemic stroke, including promoting the secretion of neurotrophic factors, mitigating inflammatory responses, inhibiting apoptosis, reducing excitotoxicity, and repairing the blood-brain barrier. Furthermore, research suggests that β2-AR activation plays a role in post-stroke pneumonia. Additionally, β2-AR gene polymorphisms have been significantly associated with the risk of ischemic stroke. This article reviews the mechanisms of the β2-AR signaling pathway in ischemic stroke, aiming to provide a theoretical foundation for the prevention and treatment of this condition.