内源性二氧化硫对心肌损伤的作用及机制

The effects and mechanisms of endogenous sulfur dioxide on myocardial injury

二氧化硫(sulfur dioxide,SO2)是一种具有强烈刺激性气味的酸性气体,以往常被认为是有害物质。内源性SO2是继一氧化氮(nitric oxide,NO)、一氧化碳(carbon monoxide,CO)和硫化氢(hydrogen sulfide,H2S)之后的第四种气体信号分子,可以在心血管组织中内源性生成,并且在心血管系统调节中发挥着重要的生理和病理学作用。SO2对心功能发挥剂量依赖性的负性肌力作用,其中三磷酸腺苷敏感钾通道参与其中。SO2还能减轻各种有害刺激引起的心肌损伤,在心肌缺血-再灌注损伤和心肌肥厚中发挥重要作用,作用机制与SO2的抑制炎症和抗氧化作用有关。此外,SO2还可以抑制心肌细胞的凋亡和自噬。因此,内源性SO2在维持心血管系统的稳态中发挥重要作用。本文将围绕内源性SO2生成代谢、心血管生物学效应及对内源性SO2/天冬氨酸氨基转移酶(aspartate aminotransferase,AAT)体系介导的心肌保护作用机制进行综述。

Sulfur dioxide,an acidic gas with a strong pungent smell,used to be considered harmful.Endogenous SO2 is the fourth gas signaling molecule after nitric oxide,carbon monoxide and hydrogen sulfide.It can be produced endogenously in cardiovascular tissues and plays an important physiological and pathophysiological role in the regulation of cardiovascular system.SO2 has a dose-dependent negative inotropic effect on cardiac function,in which adenosine triphosphate sensitive potassium channels are involved.SO2 can also reduce myocardial injury caused by various harmful stimuli,and play an important role in myocardial ischemia-reperfusion injury and myocardial hypertrophy.The mechanism of action is related to the inhibition of inflammation and antioxidant effects of SO2.In addition,SO2 can inhibit the apoptosis and autophagy of cardiomyocytes.Therefore,endogenous SO2 plays an important role in maintaining the homeostasis of the cardiovascular system.This review focuses on endogenous SO2 production and metabolism,cardiovascular biological effects and myocardial protective mechanisms mediated by endogenous SO2/aspartate aminotransferase system.