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• W4229060265 abstract "Vital organ injury is one of the leading causes of global deaths. Accumulating studies have demonstrated that dexmedetomidine (DEX) has an outstanding protective effect on multiple organs for its antiinflammatory and antiapoptotic properties, while the underlying molecular mechanism is not clearly understood. Autophagy, an adaptive catabolic process, has been found to play a crucial role in the organ-protective effects of DEX. Herein, we present a first attempt to summarize all the evidence on the proposed roles of autophagy in the action of DEX protecting against vital organ injuries via a comprehensive review. We found that most of the relevant studies (17/24, 71%) demonstrated that the modulation of autophagy was inhibited under the treatment of DEX on vital organ injuries (e.g. brain, heart, kidney, and lung), but several studies suggested that the level of autophagy was dramatically increased after administration of DEX. Albeit not fully elucidated, the underlying mechanisms governing the roles of autophagy involve the antiapoptotic properties, inhibiting inflammatory response, removing damaged mitochondria, and reducing oxidative stress, which might be facilitated by the interaction with multiple associated genes (i.e., hypoxia inducible factor-1α, p62, caspase-3, heat shock 70 kDa protein, and microRNAs) and signaling cascades (i.e., mammalian target of rapamycin, nuclear factor-kappa B, and c-Jun N-terminal kinases pathway). The authors conclude that DEX hints at a promising strategy in the management of vital organ injuries, while autophagy is crucially involved in the protective effect of DEX." @default.
• W4229060265 created "2022-05-08" @default.
• W4229060265 creator A5001506483 @default.
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• W4229060265 date "2022-05-04" @default.
• W4229060265 modified "2023-09-29" @default.
• W4229060265 title "Protective effects of dexmedetomidine in vital organ injury: crucial roles of autophagy" @default.
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• W4229060265 doi "https://doi.org/10.1186/s11658-022-00335-7" @default.
• W4229060265 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35508984" @default.
• W4229060265 hasPublicationYear "2022" @default.
• W4229060265 type Work @default.
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