Autophagy is a self-eating cellular catabolic pathway, through which long-lived proteins, damaged organelles and misfolded proteins are degraded and recycled for the maintenance of cellular homeostasis and normal cellular functions. Autophagy plays an important homeostatic role in the regulation of cell survival. Accumulating evidence shows that autophagy is activated in various cell types in the brain such as neurons, glia cells, and brain microvascular cells upon ischemic stroke. However, the exact role and molecular mechanisms of autophagy process that is implicated in ischemic stroke have yet to be elucidated. This review aims to provide a comprehensive view of the regulation of autophagy in neurons, glia cells, and brain microvascular cells in response to ischemia stress. We also review the recent advance on the understanding of the involvement of autophagy in the pathological process during cerebral ischemic preconditioning, perconditioning and postconditioning. We propose a crosstalk between autophagy, necroptosis, and apoptosis that contribute to ischemic stroke. In addition, we discuss the interactions between autophagy and oxidative stress, mitochondrial dysfunction and endoplasmic reticulum stress.

自噬是一种自我饮食的细胞分解代谢途径，长寿蛋白质，受损细胞器和错误折叠的蛋白质可通过该途径降解并循环利用，以维持细胞稳态和正常细胞功能。自噬在调节细胞存活中起着重要的稳态作用。越来越多的证据表明，缺血性中风后大脑中各种细胞类型（例如神经元，神经胶质细胞和脑微血管细胞）中的自噬被激活。然而，尚不清楚与缺血性中风有关的自噬过程的确切作用和分子机制。这篇综述旨在提供对缺血应激引起的神经元，神经胶质细胞和脑微血管细胞自噬调控的全面综述。我们还回顾了对自噬在脑缺血预适应，过适应和后适应过程中病理过程中参与的理解的最新进展。我们提出自噬，坏死病和凋亡之间的相声，这有助于缺血性中风。此外，我们讨论了自噬与氧化应激，线粒体功能障碍和内质网应激之间的相互作用。