REVIEW article
Front. Pharmacol.
Sec. Experimental Pharmacology and Drug Discovery
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1605363
The protective effect and mechanism of dexmedetomidine in inhibiting ferroptosis
Provisionally accepted
Xinyi REN1*
Ran Wang2- 1Kunshan Traditional Chinese Medicine Hospital, Kunshan, China
- 2Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China
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ABSTRACT Dexmedetomidine (DEX) is a highly selective α2-Adrenergic Receptor (α2-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.
Keywords: Dexmedetomidine, ferroptosis, α2-AR agonist, Oxidative Stress, Iron Overload
Received: 03 Apr 2025; Accepted: 21 Aug 2025.
Copyright: © 2025 REN and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Xinyi REN, Kunshan Traditional Chinese Medicine Hospital, Kunshan, China
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