基于cGAS-STING通路和突触融合蛋白17介导的自噬在脑缺血再灌注损伤中的作用研究进展 Research Progress on the Role of cGAS-STING Pathway and Syntaxin 17 Mediated Autophagy in Cerebral Ischemia-Reperfusion Injury

急性缺血性卒中后，脑缺血再灌注损伤（cerebral ischemia-reperfusion injury，CIRI）可进一步损伤患者的神经功能，影响其预后。自噬在CIRI的病理过程中是一把“双刃剑”，其不同的激活程度以及在CIRI的不同时期，可对脑组织产生保护或损伤的相反作用。环鸟苷酸-腺苷酸合酶（cyclic guanosine monophosphate-adenosine monophosphate synthase，cGAS）-干扰素基因刺激因子（stimulator of interferon gene，STING）通路是先天免疫中重要的效应通路，突触融合蛋白17（syntaxin 17，STX17）是可溶性N-乙基顺丁烯二酰亚胺敏感性因子附着蛋白受体亚家族成员，两者在CIRI过程中对细胞自噬和线粒体自噬均具有重要的调节作用。本文对cGAS-STING通路和STX17在CIRI中调控自噬的机制及其相互关系进行综述，以期为CIRI的干预提供新的思路和依据。 Abstract: After acute ischemic stroke, cerebral ischemia-reperfusion injury (CIRI) can further damage the neurological function of patients and affect their prognosis. Autophagy is a “double-edged sword” in the pathological process of CIRI. The varying stages and degrees of activation of CIRI can have opposing effects, either protecting or damaging brain tissue. The cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon gene (STING) pathway is an important pattern recognition and effector pathway in the innate immune response. Syntaxin 17 (STX17) is a member of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor subfamily. Both play significant regulatory roles in autophagy and mitophagy during the CIRI process. This article reviews the mechanisms and interrelationships between the cGAS-STING pathway and STX17 in regulating autophagy during CIRI, aiming to provide new ideas and evidence for the intervention of CIRI.