The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.
The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.
复制标题
脓毒症后全身炎症反应导致脑损伤的关键驱动因素：小胶质细胞和神经炎症。
DOI：
10.1007/s12035-022-03148-z
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发表时间：
2023-03
影响因子：
5.1
通讯作者：
Gong, Ye
中科院分区：
文献类型：
--
作者：
Xin, Yuewen;Tian, Mi;Deng, Shuixiang;Li, Jiaying;Yang, Miaoxian;Gao, Jianpeng;Pei, Xu;Wang, Yao;Tan, Jiaying;Zhao, Feng;Gao, Yanqin;Gong, Ye
关键词：
脓毒症是全世界重症监护病房住院和死亡的主要原因。大多数存活的患者表现出急性或慢性精神障碍，即败血症相关脑病（SAE）。虽然在过去的二十年中积累的研究主要集中在SAE的发病机制上，但还缺乏专门针对SAE炎症机制的回顾性研究的系统综述。本文综述了近年来神经炎症领域的研究进展，并对SAE中小胶质细胞的活化进行了阐述。小胶质细胞的激活主导了神经炎症。随着基因表达谱的改变，小胶质细胞在SAE的所有阶段都表现出异质特征。在这里，我们总结了败血症后的全身性炎症以及小胶质细胞多样性与神经炎症的关系。此外，还回顾了一系列与神经炎症相关的功能障碍，以说明SAE的可能机制。此外，本文还总结了一些有前景的药物或非药物治疗策略，特别是针对神经炎症或小胶质细胞的治疗策略。总的来说，阐明神经炎症与SAE相关精神障碍之间的重要关系将显著提高我们对SAE病理生理机制的理解，从而为旨在抑制神经炎症的SAE治疗提供潜在靶点。
Sepsis is a leading cause of intensive care unit admission and death worldwide. Most surviving patients show acute or chronic mental disorders, which are known as sepsis-associated encephalopathy (SAE). Although accumulating studies in the past two decades focused on the pathogenesis of SAE, a systematic review of retrospective studies which exclusively focuses on the inflammatory mechanisms of SAE has been lacking yet. This review summarizes the recent advance in the field of neuroinflammation and sheds light on the activation of microglia in SAE. Activation of microglia predominates neuroinflammation. As the gene expression profile changes, microglia show heterogeneous characterizations throughout all stages of SAE. Here, we summarize the systemic inflammation following sepsis and also the relationship of microglial diversity and neuroinflammation. Moreover, a collection of neuroinflammation-related dysfunction has also been reviewed to illustrate the possible mechanisms for SAE. In addition, promising pharmacological or non-pharmacological therapeutic strategies, especially those which target neuroinflammation or microglia, are also concluded in the final part of this review. Collectively, clarification of the vital relationship between neuroinflammation and SAE-related mental disorders would significantly improve our understanding of the pathophysiological mechanisms in SAE and therefore provide potential targets for therapies of SAE aimed at inhibiting neuroinflammation.
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影响因子：
120.7
作者：
Boomer, Jonathan S.;To, Kathleen;Chang, Kathy C.;Takasu, Osamu;Osborne, Dale F.;Walton, Andrew H.;Bricker, Traci L.;Jarman, Stephen D., II;Kreisel, Daniel;Krupnick, Alexander S.;Srivastava, Anil;Swanson, Paul E.;Green, Jonathan M.;Hotchkiss, Richard S.
通讯作者：
Hotchkiss, Richard S.
DOI：
10.1097/shk.0000000000000463
发表时间：
2016-03
期刊：
Shock (Augusta, Ga.)
影响因子：
--
作者：
Arulkumaran N;Deutschman CS;Pinsky MR;Zuckerbraun B;Schumacker PT;Gomez H;Gomez A;Murray P;Kellum JA;ADQI XIV Workgroup
通讯作者：
ADQI XIV Workgroup
影响因子：
5.3
作者：
Chakravarty, S;Herkenham, M
通讯作者：
Herkenham, M
影响因子：
8.8
作者：
Barr, Juliana;Fraser, Gilles L.;Jaeschke, Roman
通讯作者：
Jaeschke, Roman
影响因子：
25
作者：
Butovsky, Oleg;Jedrychowski, Mark P.;Moore, Craig S.;Cialic, Ron;Lanser, Amanda J.;Gabriely, Galina;Koeglsperger, Thomas;Dake, Ben;Wu, Pauline M.;Doykan, Camille E.;Fanek, Zain;Liu, LiPing;Chen, Zhuoxun;Rothstein, Jeffrey D.;Ransohoffl, Richard M.;Gygi, Steven P.;Antel, Jack P.;Weiner, Howard L.
通讯作者：
Weiner, Howard L.