Mechanisms Underlying the Renal Protective Effects of Dexmedetomidine

Purpose of Review This review summarizes the recent literature on the renoprotective mechanisms of Dexmedetomidine (Dex). Recent Findings Dex, an α2-adrenergic agonist with sedative, analgesic, and anti-inflammatory properties, has demonstrated efficacy in various surgical settings. The renoprotective mechanisms of Dex includes suppression of reactive oxygen species (ROS) production, apoptosis, and inflammatory cytokines. Dex also regulates pathways such as TLR4/MyD88/ERK, α2-adrenoreceptor/AMPK/mTOR, and PI3K-Akt. Additionally, Dex’s inhibition of KDM5A, and regulation of BMP-7 and HDAC2/HDAC5, attenuates renal damage. It inhibits ferroptosis-mediated renal injury, modulates vasoreactivity to maintain hemodynamics, and improves renal blood flow post-surgery. Summary The renoprotective mechanisms of Dex involve inhibition of oxidative stress and apoptosis, modulation of inflammatory cytokine responses, and vasoreactivity. Dex shows promise in AKI prevention and management across diverse surgical contexts, highlighting its value in perioperative care.