Abstract: Background Renal ischemia/reperfusion injury (I/RI) is one of the most important postoperative complications affecting the recovery and survival of patients. It has been shown that dexmedetomidine (Dex) mitigates renal I/RI. Objective To review the potential mechanisms underlying the protective effect of Dex on renal I/RI. Content Accumulating evidence shows that Dex may protect the kidney through controlling several cellular events and regulating multiple signal transduction pathways, which are mobilized in renal I/RI. In addition to its antioxidant property to scavenge oxygen free radical and reduce oxidative stress, Dex can also inhibit inflammation and apoptosis, and improve mitochondrial function. The potential signal transduction pathways involved in the benefits of Dex to renal I/RI include janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3), Toll-like receptors 4 (TLR4), phosphatidylinositide 3 kinase/protein kinase B (PI3K/Akt), and silent information regulator 2 homolog 3 (SIRT3), etc. Trend Further investigations should be conducted to elucidate the potential targets of Dex, which are able to be transformed for clinical intervention and treatment of renal I/RI.
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