The protective effect and mechanism of dexmedetomidine in inhibiting ferroptosis

Dexmedetomidine (DEX) is a highly selective α 2 -Adrenergic Receptor (α 2 -AR) agonist which inhibits sympathetic nerve activity, and has been shown to have a wide range of sedative, analgesic, anesthetic and other effects, as well as reducing inflammation and exerting neuroprotective functions. Researches show that DEX provides an advantage of protecting vital organs from injury, such as myocardial, kidney or cerebral injury. Nowadays, the regulatory effect of DEX in ferroptosis has become a headline in current researches. Ferroptosis is a type of programmed cell death discovered in recent years and is considered to play an important role in mediating the onset and progression of diseases. The aim of this review is to further clarify the role and mechanism of DEX in inhibiting ferroptosis.