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急性肺损伤中程序性细胞死亡的调控:从发病机制到治疗

Regulated programmed cell death in acute lung injury: from pathogenesis to therapy.

作者信息

Liu Shi-Wen, Chen Yi-Jian, Liu Yi, Zhou Wen, Liu Xuan

机构信息

Department of Anesthesiology, Ganzhou People's Hospital, Ganzhou, Jiangxi, China.

Department of Anesthesiology, Ganzhou Hospital-Nanfang Hospital, Southern Medical University, Ganzhou, Jiangxi, China.

出版信息

Front Immunol. 2025 Jul 23;16:1630015. doi: 10.3389/fimmu.2025.1630015. eCollection 2025.


DOI:10.3389/fimmu.2025.1630015
PMID:40771815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12325065/
Abstract

Acute lung injury (ALI) is a common, life-threatening lung disease with a high mortality rate, primarily associated with acute and severe inflammation of the lungs. There are many factors that lead to ALI, and abnormally advanced regulated programmed cell death (RCD) is considered to be an important process in the pathological process of ALI. Various forms of RCD have been discovered in recent years, including apoptosis, necroptosis, autophagy, ferroptosis and pyroptosis. Unlike necrosis, RCD is an active cell death mediated by a series of gene expression events that is essential for eliminating unnecessary and damaged cells as well as defense mechanisms. Previous studies have shown that RCD has a strong relationship with ALI. Therefore, it is important to describe the role of RCD not only to enhance our understanding of the pathophysiological processes of ALI, but also to improve the functional recovery after ALI. This review reviews the roles and mechanisms of various RCD (apoptosis, pyroptosis, necroptosis, ferroptosis and autophagy) in ALI, and discusses the associations among various types of RCD. The aim is to explore the molecular mechanism behind SALI and find new targets for the treatment of ALI. This review will help us understand the various functions and mechanisms of RCD in the pathological process of ALI, and help us to treat various ALI of unknown etiology.

摘要

急性肺损伤(ALI)是一种常见的、危及生命的肺部疾病,死亡率高,主要与肺部的急性严重炎症有关。导致ALI的因素众多,异常过度的程序性细胞死亡(RCD)被认为是ALI病理过程中的一个重要过程。近年来发现了多种形式的RCD,包括凋亡、坏死性凋亡、自噬、铁死亡和焦亡。与坏死不同,RCD是由一系列基因表达事件介导的主动细胞死亡,对于清除不必要的和受损的细胞以及防御机制至关重要。先前的研究表明,RCD与ALI密切相关。因此,描述RCD的作用不仅对于增强我们对ALI病理生理过程的理解很重要,而且对于改善ALI后的功能恢复也很重要。本综述回顾了各种RCD(凋亡、焦亡、坏死性凋亡、铁死亡和自噬)在ALI中的作用和机制,并讨论了各种类型RCD之间的关联。目的是探索SALI背后的分子机制,并找到治疗ALI的新靶点。本综述将有助于我们了解RCD在ALI病理过程中的各种功能和机制,并有助于我们治疗各种病因不明的ALI。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/4d2e1e7dc9eb/fimmu-16-1630015-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/2ee744812595/fimmu-16-1630015-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/6dbd2e5d219e/fimmu-16-1630015-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/e547fc202082/fimmu-16-1630015-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/0c57d0e791e6/fimmu-16-1630015-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/ccaac3386458/fimmu-16-1630015-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/7749733ec02f/fimmu-16-1630015-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/06bec95a922e/fimmu-16-1630015-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/4d2e1e7dc9eb/fimmu-16-1630015-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/2ee744812595/fimmu-16-1630015-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/6dbd2e5d219e/fimmu-16-1630015-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/e547fc202082/fimmu-16-1630015-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/0c57d0e791e6/fimmu-16-1630015-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/ccaac3386458/fimmu-16-1630015-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/7749733ec02f/fimmu-16-1630015-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/06bec95a922e/fimmu-16-1630015-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5147/12325065/4d2e1e7dc9eb/fimmu-16-1630015-g008.jpg

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本文引用的文献

[1]
Isoginkgetin inhibits macrophage activation and ferroptosis of lung epithelial cells under lipopolysaccharide-induced immunological stress via HOXA5-dependent inhibition of the TLR4/NF-κΒ signaling pathway.

Toxicol Appl Pharmacol. 2025-9

[2]
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J Nanobiotechnology. 2025-2-27

[3]
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Commun Biol. 2025-2-3

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J Inflamm Res. 2024-12-21

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Front Immunol. 2024-11-15

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[10]
Phillyrin prevents sepsis-induced acute lung injury through inhibiting the NLRP3/caspase-1/GSDMD-dependent pyroptosis signaling pathway.

Acta Biochim Biophys Sin (Shanghai). 2024-10-10

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