右美托咪定改善心肌缺血-再灌注损伤作用机制的研究进展

Research progress on the mechanism of dexmedetomidine in improving myocardial ischemia-reperfusion injury

中文关键词: 右美托咪定  心肌缺血-再灌注损伤  信号通路  作用机制

英文关键词: Dexmedetomidine  Myocardial ischemia-reperfusion injury  Signal pathway  Mechanism of action

中文摘要:

      心肌缺血-再灌注损伤（MIRI）是心血管疾病中的一种常见且严重的并发症，是心脏病学领域的重要且具有挑战性的临床问题。MIRI的机制涉及氧化应激、炎症反应和细胞凋亡等因素。右美托咪定作为一种选择性α₂肾上腺素能受体激动药，近年来在心肌保护方面显示出了潜在的治疗效果。本文重点探讨了右美托咪定通过干预PI3K/Akt信号通路、MAPK信号通路、NF-κB信号通路、mTOR信号通路、Nrf2信号通路、AMPK信号通路、JAK/STAT信号通路从而显著减轻MIRI的机制与作用，旨在为临床上MIRI的防治提供策略和后续研究提供参考。

英文摘要:

      Myocardial ischemia-reperfusion injury (MIRI) is a common and serious complication of cardiovascular diseases, which is an important and challenging clinical problem in the field of cardiology. The mechanism of MIRI involves factors such as oxidative stress, inflammatory response, and apoptosis. Dexmedetomidine, a selective α₂ adrenergic receptor agonist, has shown significant potential therapeutic effects in myocardial protection in recent years. This article focuses on the mechanism and effect of dexmedetomideine in reducing MIRI by interfering with PI3K/Akt signaling pathway, MAPK signaling pathway, NF-κB signaling pathway, mTOR signaling pathway, JAK/STAT signaling pathway, AMPK signaling pathway, and Nrf2 signaling pathway. The purpose of this article is to provide theoretical basis and potential therapeutic strategies for the prevention and treatment of clinical MIRI, as well as to provide research directions for follow-up research.