自发性蛛网膜下腔出血早期脑损伤中自噬的研究进展

Research progress of autophagy in early brain injury of spontaneous subarachnoid hemorrhage

自发性蛛网膜下腔出血(SAH)是一种神经外科常见疾病,具有高病死率和高致残率,而出血后早期脑损伤(EBI)是影响预后的重要因素之一。虽然通过药物、手术及介入治疗取得了一定疗效,但SAH患者神经功能的恢复仍不理想。自噬是一种维持内稳态的机制,越来越多的研究表明自噬在SAH后EBI中起着重要作用,并通过磷脂酰肌醇3激酶/蛋白激酶B/雷帕霉素靶蛋白(PI3K/Akt/mTOR)、腺苷酸活化蛋白激酶(AMP)K/mTOR等信号通路抑制神经细胞凋亡,但其具体机制尚未不明确。本文就SAH的病理生理机制和自噬的信号通路进行综述,以期为SAH药物研发和临床治疗方案选择提供参考。

Spontaneous subarachnoid hemorrhage(SAH)is a common neurosurgical disease with high mortality rate and disability rate.Early brain injury(EBI)after SAH is one of the important factors affecting the prognosis.Although some curative effects have been achieved through drugs,surgery and interventional therapy,the recovery of neurological function in SAH patients is still not ideal.Autophagy is a mechanism of maintaining homeostasis.More and more studies have shown that autophagy plays an important role in EBI after SAH,and inhibits neuronal apoptosis through phosphatidylinositol 3 kinase/protein kinase B/rapamycin target protein(PI3K/Akt/mTOR),adenosine monophosphate activated protein kinase(AMP)K/mTOR and other signaling pathways,but the specific mechanism is not clear.This article reviewed the pathophysiological mechanism and autophagy signaling pathway of SAH in order to provide references for the research and development of SAH drugs and clinical treatment scheme selection.