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慢性阻塞性肺疾病中线粒体的细胞和分子生物学。

Cellular and Molecular Biology of Mitochondria in Chronic Obstructive Pulmonary Disease.

机构信息

Department of Respiratory Therapy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, #123, Ta-Pei Road, Niaosong District, Kaohsiung 833, Taiwan.

出版信息

Int J Mol Sci. 2024 Jul 16;25(14):7780. doi: 10.3390/ijms25147780.

DOI:10.3390/ijms25147780
PMID:39063022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11276859/
Abstract

Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder characterized by enduring airflow limitation and chronic inflammation. Growing evidence highlights mitochondrial dysfunction as a critical factor in COPD development and progression. This review explores the cellular and molecular biology of mitochondria in COPD, focusing on structural and functional changes, including alterations in mitochondrial shape, behavior, and respiratory chain complexes. We discuss the impact on cellular signaling pathways, apoptosis, and cellular aging. Therapeutic strategies targeting mitochondrial dysfunction, such as antioxidants and mitochondrial biogenesis inducers, are examined for their potential to manage COPD. Additionally, we consider the role of mitochondrial biomarkers in diagnosis, evaluating disease progression, and monitoring treatment efficacy. Understanding the interplay between mitochondrial biology and COPD is crucial for developing targeted therapies to slow disease progression and improve patient outcomes. Despite advances, further research is needed to fully elucidate mitochondrial dysfunction mechanisms, discover new biomarkers, and develop targeted therapies, aiming for comprehensive disease management that preserves lung function and enhances the quality of life for COPD patients.

摘要

慢性阻塞性肺疾病(COPD)是一种以持续气流受限和慢性炎症为特征的进行性呼吸系统疾病。越来越多的证据强调线粒体功能障碍是 COPD 发生和发展的关键因素。本综述探讨了 COPD 中线粒体的细胞和分子生物学,重点关注结构和功能的变化,包括线粒体形态、行为和呼吸链复合物的改变。我们讨论了对细胞信号通路、细胞凋亡和细胞衰老的影响。探讨了靶向线粒体功能障碍的治疗策略,如抗氧化剂和线粒体生物发生诱导剂,以评估其在 COPD 管理中的潜在应用。此外,我们还考虑了线粒体生物标志物在诊断、评估疾病进展和监测治疗效果中的作用。了解线粒体生物学与 COPD 的相互作用对于开发靶向治疗以减缓疾病进展和改善 COPD 患者的预后至关重要。尽管已经取得了进展,但仍需要进一步的研究来充分阐明线粒体功能障碍的机制,发现新的生物标志物,并开发靶向治疗方法,以实现全面的疾病管理,保持肺功能并提高 COPD 患者的生活质量。

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Redox Biol. 2024 Apr;70:103049. doi: 10.1016/j.redox.2024.103049. Epub 2024 Jan 20.
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Therapeutic Targets and Precision Medicine in COPD: Inflammation, Ion Channels, Both, or Neither?COPD 的治疗靶点和精准医学:炎症、离子通道,还是两者兼有?
Int J Mol Sci. 2023 Dec 11;24(24):17363. doi: 10.3390/ijms242417363.
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Molecular Mechanisms and the Interplay of Important Chronic Obstructive Pulmonary Disease Biomarkers Reveals Novel Therapeutic Targets.慢性阻塞性肺疾病重要生物标志物的分子机制及其相互作用揭示了新的治疗靶点。
ACS Omega. 2023 Nov 20;8(49):46376-46389. doi: 10.1021/acsomega.3c07480. eCollection 2023 Dec 12.
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Reactive oxygen species, toxicity, oxidative stress, and antioxidants: chronic diseases and aging.活性氧物种、毒性、氧化应激和抗氧化剂:慢性疾病和衰老。
Arch Toxicol. 2023 Oct;97(10):2499-2574. doi: 10.1007/s00204-023-03562-9. Epub 2023 Aug 19.
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