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线粒体功能障碍诱导急性肺损伤细胞焦亡的研究进展。

Research progress of mitochondrial dysfunction induced pyroptosis in acute lung injury.

机构信息

School of Pharmacy, Southwest Medical University, Luzhou, 646000, China.

Department of Gastroenterology, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.

出版信息

Respir Res. 2024 Nov 7;25(1):398. doi: 10.1186/s12931-024-03028-1.

DOI:10.1186/s12931-024-03028-1
PMID:39511593
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11545853/
Abstract

Acute lung injury (ALI) is a common critical respiratory disease in clinical practice, especially in the ICU, with a high mortality rate. The pathogenesis of ALI is relatively complex, mainly involving inflammatory response imbalance, oxidative stress, cell apoptosis, and other aspects. However, currently, the treatment measures taken based on the above mechanisms have not had significant effects. Recent research shows that mitochondrial dysfunction and pyroptosis play an important role in ALI, but there is not much analysis on the relationship between mitochondrial dysfunction and pyroptosis at present. This article reviews the situation of mitochondrial dysfunction in ALI, pyroptosis in ALI, whether mitochondrial dysfunction is related to pyroptosis in ALI, and how to do so, and further analyzes the relationship between them in ALI. This review describes how to alleviate mitochondrial dysfunction, and then suppress the associated immunological pyroptosis, providing new ideas for the clinical treatment of ALI.

摘要

急性肺损伤(ALI)是临床实践中常见的危急呼吸系统疾病,尤其在 ICU 中,其死亡率较高。ALI 的发病机制较为复杂,主要涉及炎症反应失衡、氧化应激、细胞凋亡等多个方面。但目前基于上述机制所采取的治疗措施并未取得显著效果。近期研究表明,线粒体功能障碍和细胞焦亡在 ALI 中发挥着重要作用,但目前对于线粒体功能障碍与细胞焦亡之间的关系分析较少。本文就 ALI 中的线粒体功能障碍、ALI 中的细胞焦亡、线粒体功能障碍是否与 ALI 中的细胞焦亡相关及如何相关进行综述,并进一步分析它们在 ALI 中的关系。该综述描述了如何缓解线粒体功能障碍,进而抑制相关的免疫性细胞焦亡,为 ALI 的临床治疗提供新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc69/11545853/dcb9ba0fe6bb/12931_2024_3028_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc69/11545853/f814f76af927/12931_2024_3028_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc69/11545853/51a256feda8d/12931_2024_3028_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc69/11545853/dcb9ba0fe6bb/12931_2024_3028_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc69/11545853/f814f76af927/12931_2024_3028_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc69/11545853/51a256feda8d/12931_2024_3028_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc69/11545853/dcb9ba0fe6bb/12931_2024_3028_Fig3_HTML.jpg

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Mitochondrial network dynamics in pulmonary disease: Bridging the gap between inflammation, oxidative stress, and bioenergetics.
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