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自噬与慢性脑缺血炎症的相互作用

Crosstalk Between Autophagy and Inflammation in Chronic Cerebral Ischaemia.

机构信息

Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases of Ministry of Education, Gannan Medical University, 1st Hexie Road, Ganzhou, 341000, China.

Ganzhou Key Laboratory of Neuroinflammation Research, Gannan Medical University, 1st Hexie Road, Ganzhou, 341000, China.

出版信息

Cell Mol Neurobiol. 2023 Aug;43(6):2557-2566. doi: 10.1007/s10571-023-01336-6. Epub 2023 Mar 23.

DOI:10.1007/s10571-023-01336-6
Abstract

Chronic cerebral ischaemia (CCI) is a high-incidence cardiovascular and cerebrovascular disease that is very common in clinical practice. Although many pathogenic mechanisms have been explored, there is still great controversy among neuroscientists regarding the pathogenesis of CCI. Therefore, it is important to elucidate the mechanisms of CCI occurrence and progression for the prevention and treatment of ischaemic cerebrovascular disorders. Autophagy and inflammation play vital roles in CCI, but the relationship between these two processes in this disease remains unknown. Here, we review the progression and discuss the functions, actions and pathways of autophagy and inflammation in CCI, including a comprehensive view of the transition from acute disease to CCI through ischaemic repair mechanisms. This review may provide a reference for future research and treatment of CCI. Schematic diagram of the interplay between autophagy and inflammation in CCI. CCI lead to serious, life-threatening complications. This review summarizes two factors in CCI, including autophagy and inflammation, which have been focused for the mechanisms of CCI. In short, the possible points of intersection are shown in the illustration. CCI, Chronic cerebral ischaemia; ER stress, Endoplasmic reticulum stress; ROS, Reactive oxygen species.

摘要

慢性脑缺血(CCI)是一种高发的心血管和脑血管疾病,在临床实践中非常常见。尽管已经探索了许多发病机制,但神经科学家们对于 CCI 的发病机制仍存在很大争议。因此,阐明 CCI 发生和进展的机制对于缺血性脑血管疾病的预防和治疗非常重要。自噬和炎症在 CCI 中起着至关重要的作用,但在这种疾病中,这两个过程之间的关系尚不清楚。在这里,我们综述了 CCI 的进展,并讨论了自噬和炎症在 CCI 中的作用、作用和途径,包括通过缺血修复机制从急性疾病向 CCI 转变的全面观点。这篇综述可能为未来 CCI 的研究和治疗提供参考。CCI 中自噬和炎症相互作用的示意图。CCI 导致严重的、危及生命的并发症。本综述总结了 CCI 中的两个因素,包括自噬和炎症,这些因素是 CCI 机制的重点。简而言之,图中显示了可能的交点。CCI,慢性脑缺血;ER 应激,内质网应激;ROS,活性氧。

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Behav Sci (Basel). 2022 Aug 14;12(8):287. doi: 10.3390/bs12080287.
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Ablation of Siglec-E augments brain inflammation and ischemic injury.Siglec-E 的消融增强了大脑炎症和缺血性损伤。
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抑制内质网应激可改善与抑制 IRE1α/TRAF2/ASK1/JNK 依赖性细胞凋亡相关的慢性缺血性海马损伤。
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Activated Drp1 regulates p62-mediated autophagic flux and aggravates inflammation in cerebral ischemia-reperfusion via the ROS-RIP1/RIP3-exosome axis.激活的 Drp1 通过 ROS-RIP1/RIP3-外泌体轴调节 p62 介导的自噬流,并加重脑缺血再灌注中的炎症反应。
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Pre- and post-conditioning with poly I:C exerts neuroprotective effect against cerebral ischemia injury in animal models: A systematic review and meta-analysis.聚肌苷酸胞苷酸预处理和后处理对动物模型脑缺血损伤发挥神经保护作用:系统评价和荟萃分析。
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