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自噬对细胞焦亡的调控:脓毒症中的作用机制及医学意义。

Autophagy Regulation on Pyroptosis: Mechanism and Medical Implication in Sepsis.

机构信息

Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100730, China.

出版信息

Mediators Inflamm. 2021 Jun 24;2021:9925059. doi: 10.1155/2021/9925059. eCollection 2021.

DOI:10.1155/2021/9925059
PMID:34257519
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8253640/
Abstract

Sepsis is defined as a life-threatening disease involving multiple organ dysfunction caused by dysregulated host responses to infection. To date, sepsis remains a dominant cause of death among critically ill patients. Pyroptosis is a unique form of programmed cell death mediated by the gasdermin family of proteins and causes lytic cell death and release of proinflammatory cytokines. Although there might be some positive aspects to pyroptosis, it is regarded as harmful during sepsis and needs to be restricted. Autophagy was originally characterized as a homeostasis-maintaining mechanism in living cells. In the past decade, its function in negatively modulating pyroptosis and inflammation during sepsis has attracted increased attention. Here, we present a comprehensive review of the regulatory effect of autophagy on pyroptosis during sepsis, including the latest advances in our understanding of the mechanism and signaling pathways involved, as well as the potential therapeutic application in sepsis.

摘要

脓毒症定义为一种危及生命的疾病,涉及宿主对感染的失调反应引起的多器官功能障碍。迄今为止,脓毒症仍然是危重病患者死亡的主要原因。细胞焦亡是一种由gasdermin 家族蛋白介导的独特的程序性细胞死亡形式,导致细胞裂解和促炎细胞因子的释放。虽然细胞焦亡可能有一些积极的方面,但在脓毒症中被认为是有害的,需要加以限制。自噬最初被描述为活细胞中维持内稳态的机制。在过去的十年中,它在负调控脓毒症中细胞焦亡和炎症的功能引起了越来越多的关注。在这里,我们全面回顾了自噬对脓毒症中细胞焦亡的调节作用,包括对相关机制和信号通路的最新理解,以及在脓毒症中的潜在治疗应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a13/8253640/d6ec10ca71d8/MI2021-9925059.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a13/8253640/dd951611c6c6/MI2021-9925059.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a13/8253640/17b99631019c/MI2021-9925059.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a13/8253640/d6ec10ca71d8/MI2021-9925059.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a13/8253640/dd951611c6c6/MI2021-9925059.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a13/8253640/17b99631019c/MI2021-9925059.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a13/8253640/d6ec10ca71d8/MI2021-9925059.003.jpg

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