摘要
缺血再灌注(IR)损伤可导致组织器官出现严重的功能障碍,显著增加患者的病死率,但其机制目前尚不完全清楚,缺乏有效的治疗手段和药物。琥珀酸盐代谢异常在IR损伤的发病机制中具有关键作用。琥珀酸盐浓度在组织器官缺血期显著升高,可作为缺血的一种代谢信号分子。再灌注期琥珀酸盐通过促进活性氧类爆发生成引起氧化损伤,并通过稳定缺氧诱导因子1α和激活琥珀酸受体1两种途径引起无菌性炎症反应。因此,深入了解琥珀酸盐代谢异常与IR损伤的关系,可能为IR损伤的防治提供新靶点。
Ischemia-reperfusion(IR)injury leads to severe dysfunction of tissues and organs and significantly increases the mortality of patients,but the mechanism is not fully understood and effective treatments and drugs are lacking.Metabolic abnormalities of succinate play a key role in the pathogenesis of IR injury.The concentration of succinate increases significantly during the tissues and organs ischemia,and can serve as a metabolic signal molecule of ischemia.During reperfusion,succinate causes oxidative damage by promoting the explosive production of reactive oxygen species,and causes aseptic inflammation by stabilizing hypoxia-inducing factor-1αand activating succinate receptor 1.Therefore,in-depth understanding of the association between metabolic abnormalities of succinate and IR injury may provide a new target for the prevention and treatment of IR injury.
作者
李成龙
彭晓伟
戚思华
LI Chenglong;PENG Xiaowei;QI Sihua(Department of Anesthesiology,the Fourth Affiliated Hospital of Harbin Medical University,Harbin 150001,China)
出处
《医学综述》
2020年第19期3843-3847,3853,共6页
Medical Recapitulate
关键词
缺血再灌注损伤
琥珀酸盐
活性氧类
炎症反应
Ischemia-reperfusion injury
Succinate
Reactive oxygen species
Inflammation
