Year: 2025
Type: article
Abstract: 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.
Source: Current anesthesiology reports
Authors: Karina M Chan, Ke Peng, Fuhai Ji, Artin Yeranossian, Julie Fowler, Xiaomei Feng
Language: English
Topic: Acute Kidney Injury Research
Subfield: Nephrology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $3,890
Funder: National Institutes of Health
OpenAlex ID: W4413314206