Autophagy is a critical cytoprotective mechanism that takes a hand in innate or adaptive immune responses. Hypoxia is a common pathophysiological mechanism that can lead to systemic pathological reactions. In recent years, the impact of hypoxia on the central nervous system has attracted more attention. In the past, autophagy was thought to be directly involved in the apoptosis of nerve cells under hypoxia. An increasing amount of evidence shows that the neuroinflammatory response plays an indispensable role in the neural damage caused by hypoxia. There are many mechanisms related to the neuroinflammatory response induced by hypoxia, among which autophagy is an important aspect, but the role of autophagy is still unclear. This article focuses on how autophagy flux of central immune cells is modified under hypoxic conditions, and how this autophagy affects neuroinflammatory response.

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自噬在缺氧诱导的神经炎症中的作用

自噬是一种重要的细胞保护机制，可参与先天性或适应性免疫反应。缺氧是一种常见的病理生理机制，可导致全身病理反应。近年来，缺氧对中枢神经系统的影响越来越受到关注。过去认为自噬直接参与了缺氧条件下神经细胞的凋亡。越来越多的证据表明，神经炎症反应在缺氧引起的神经损伤中起着不可或缺的作用。与缺氧诱导的神经炎症反应相关的机制很多，其中自噬是一个重要方面，但自噬的作用尚不清楚。本文重点介绍了在缺氧条件下如何改变中枢免疫细胞的自噬通量，