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缺血性心脏病中的线粒体自噬:分子机制与临床管理

Mitophagy in ischemic heart disease: molecular mechanisms and clinical management.

作者信息

Xu Shujuan, Wang Zihan, Guo Fan, Zhang Yehao, Peng Han, Zhang Huiyu, Liu Zixin, Cao Ce, Xin Gaojie, Chen Yuan Yuan, Fu Jianhua

机构信息

Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, 100091, China.

Department of Oral Implantology, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang, 110122, China.

出版信息

Cell Death Dis. 2024 Dec 30;15(12):934. doi: 10.1038/s41419-024-07303-3.

DOI:10.1038/s41419-024-07303-3
PMID:39737905
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11685431/
Abstract

The influence of the mitochondrial control system on ischemic heart disease has become a major focus of current research. Mitophagy, as a very crucial part of the mitochondrial control system, plays a special role in ischemic heart disease, unlike mitochondrial dynamics. The published reviews have not explored in detail the unique function of mitophagy in ischemic heart disease, therefore, the aim of this paper is to summarize how mitophagy regulates the progression of ischemic heart disease. We conclude that mitophagy affects ischemic heart disease by promoting cardiomyocyte hypertrophy and fibrosis, the progression of oxidative stress, the development of inflammation, and cardiomyocyte death, and that the specific mechanisms of mitophagy are worthy of further investigation.

摘要

线粒体控制系统对缺血性心脏病的影响已成为当前研究的主要焦点。与线粒体动力学不同,线粒体自噬作为线粒体控制系统的一个非常关键的部分,在缺血性心脏病中发挥着特殊作用。已发表的综述尚未详细探讨线粒体自噬在缺血性心脏病中的独特功能,因此,本文的目的是总结线粒体自噬如何调节缺血性心脏病的进展。我们得出结论,线粒体自噬通过促进心肌细胞肥大和纤维化、氧化应激的进展、炎症的发展以及心肌细胞死亡来影响缺血性心脏病,并且线粒体自噬的具体机制值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/2f4f2f8dceab/41419_2024_7303_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/79439dd07618/41419_2024_7303_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/1a9b3b4809ee/41419_2024_7303_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/4b989dd869e9/41419_2024_7303_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/2f4f2f8dceab/41419_2024_7303_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/79439dd07618/41419_2024_7303_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/1a9b3b4809ee/41419_2024_7303_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/4b989dd869e9/41419_2024_7303_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfb/11685431/2f4f2f8dceab/41419_2024_7303_Fig4_HTML.jpg

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本文引用的文献

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Front Neurosci. 2024 Aug 7;18:1451845. doi: 10.3389/fnins.2024.1451845. eCollection 2024.
2
Ruthenium red alleviates post-resuscitation myocardial dysfunction by upregulating mitophagy through inhibition of USP33 in a cardiac arrest rat model.钌红通过抑制心脏骤停大鼠模型中的USP33上调线粒体自噬,从而减轻复苏后心肌功能障碍。
Eur J Pharmacol. 2024 Jul 5;974:176633. doi: 10.1016/j.ejphar.2024.176633. Epub 2024 May 3.
3
巨噬细胞Notch1通过损害线粒体自噬和促进NLRP3激活来驱动脓毒症性心脏功能障碍。
Biol Direct. 2025 May 26;20(1):65. doi: 10.1186/s13062-025-00657-4.
4
The HNRNPC/CELF2 signaling pathway drives glycolytic reprogramming and mitochondrial dysfunction in drug-resistant acute myeloid leukemia.HNRNPC/CELF2信号通路驱动耐药性急性髓系白血病中的糖酵解重编程和线粒体功能障碍。
Cell Biosci. 2025 May 16;15(1):61. doi: 10.1186/s13578-025-01386-x.
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