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用天然提取物化合物调节线粒体:从实验室到慢性阻塞性肺疾病的临床治疗机遇

Modulating mitochondria with natural extract compounds: from bench to clinical therapeutic opportunities for COPD.

作者信息

Wang Qiao, Zeng Ziling, Guo Linlin, Williams Kent E, Zhang Yun, Tang Hongmei, Hu Hang, Qin Gang, Wang Kaijin, Wang Xing

机构信息

Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou, China.

Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, United States.

出版信息

Front Pharmacol. 2025 May 21;16:1531302. doi: 10.3389/fphar.2025.1531302. eCollection 2025.

DOI:10.3389/fphar.2025.1531302
PMID:40469988
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12133498/
Abstract

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease that leads to death and disability worldwide, and it is caused by hereditary and environmental factors. It is characterized by chronic inflammation, emphysema, and irreversible limitation of airflow. Dual or triple therapy with a traditional approach can provide relief from COPD symptoms by reducing the frequency and severity of the outbreaks, but there are no current therapies to reverse the long-term decline in lung function. Although ICS rescue inhalers demonstrate efficacy in acute attacks, these cannot be utilized for chronic management of COPD due to adverse effects. Therefore, novel agents and therapeutic strategies are urgently needed to address this disease. It is believed that malfunctioning mitochondria are associated with COPD pathogenesis, contributing to inflammation, apoptosis, and cellular senescence. A better understanding of these mechanisms could provide novel therapeutic approaches for maintaining lung and skeletal muscle function. Many natural extract compounds show therapeutic potential for COPD and are associated with few adverse reactions. Notably, these natural compounds can improve mitochondrial function and exhibit a variety of anti-inflammatory, antioxidant, and immunomodulatory properties. In this review, we systemically summarize the pathogenic role of impaired mitochondria in COPD and the potential mechanisms by which natural extract compounds may ameliorate these impairments.

摘要

慢性阻塞性肺疾病(COPD)是一种在全球范围内导致死亡和残疾的慢性呼吸道疾病,由遗传和环境因素引起。其特征为慢性炎症、肺气肿以及气流的不可逆受限。采用传统方法进行双重或三重治疗可通过减少发作频率和严重程度来缓解COPD症状,但目前尚无疗法能逆转肺功能的长期下降。尽管吸入性糖皮质激素(ICS)急救吸入器在急性发作中显示出疗效,但由于不良反应,这些药物不能用于COPD的长期管理。因此,迫切需要新型药物和治疗策略来应对这种疾病。据信,线粒体功能异常与COPD发病机制相关,会导致炎症、细胞凋亡和细胞衰老。更好地理解这些机制可为维持肺和骨骼肌功能提供新的治疗方法。许多天然提取物化合物显示出对COPD的治疗潜力,且不良反应较少。值得注意的是,这些天然化合物可改善线粒体功能,并具有多种抗炎、抗氧化和免疫调节特性。在本综述中,我们系统地总结了线粒体功能受损在COPD中的致病作用以及天然提取物化合物可能改善这些损伤的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/c7fa64663213/fphar-16-1531302-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/f253053843c5/fphar-16-1531302-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/3c9a8c1e0164/fphar-16-1531302-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/6a7172bc81fd/fphar-16-1531302-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/c7fa64663213/fphar-16-1531302-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/f253053843c5/fphar-16-1531302-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/3c9a8c1e0164/fphar-16-1531302-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/6a7172bc81fd/fphar-16-1531302-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9281/12133498/c7fa64663213/fphar-16-1531302-g004.jpg

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本文引用的文献

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Nat Commun. 2024 Jun 18;15(1):5199. doi: 10.1038/s41467-024-49597-z.
2
Salubrinal promotes phospho-eIF2α-dependent activation of UPR leading to autophagy-mediated attenuation of iron-induced insulin resistance.沙利度胺促进磷酸化 eIF2α 依赖性 UPR 的激活,导致自噬介导的铁诱导的胰岛素抵抗减弱。
Mol Metab. 2024 May;83:101921. doi: 10.1016/j.molmet.2024.101921. Epub 2024 Mar 26.
3
The role of endoplasmic reticulum-mitochondria-associated membranes in diabetic kidney disease.
内质网-线粒体相关膜在糖尿病肾病中的作用。
Cardiovasc Res. 2024 Feb 17;119(18):2875-2883. doi: 10.1093/cvr/cvad190.
4
Role of mitochondrial fusion proteins MFN2 and OPA1 on lung cellular senescence in chronic obstructive pulmonary disease.线粒体融合蛋白MFN2和OPA1在慢性阻塞性肺疾病肺细胞衰老中的作用
Respir Res. 2023 Dec 18;24(1):319. doi: 10.1186/s12931-023-02634-9.
5
The Activation of M1 Macrophages is Associated with the JNK-m6A-p38 Axis in Chronic Obstructive Pulmonary Disease.M1 巨噬细胞的激活与慢性阻塞性肺疾病中的 JNK-m6A-p38 轴相关。
Int J Chron Obstruct Pulmon Dis. 2023 Oct 6;18:2195-2206. doi: 10.2147/COPD.S420471. eCollection 2023.
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Mol Metab. 2023 Dec;78:101816. doi: 10.1016/j.molmet.2023.101816. Epub 2023 Oct 10.
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Phytother Res. 2023 Sep;37(9):4251-4264. doi: 10.1002/ptr.7905. Epub 2023 May 30.
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