线粒体稳态在慢性鼻窦炎发病机制中的作用
The Role of Mitochondrial Homeostasis in the Pathogenesis of Chronic Rhinosinusitis.
文献信息
| PMID | 42985996 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Babak Ghalehbaghi |
| 作者单位 | ENT and Head and Neck Research Center and Department, School of Medicine, The Five Senses Health Institute, Iran University of Medical Sciences, Tehran, Iran. |
| 期刊 | Immunity, inflammation and disease |
| SCI 分区 | Q2 |
| IF | 3.2 |
| 研究类型 | 综述 Meta · 基础／转化 |
| 所属专科 | 鼻科 |
中文摘要
背景： 慢性鼻窦炎（CRS）是一种常见临床疾病，以鼻腔和鼻窦黏膜的持续性炎症为特征。尽管炎症内型已被充分描述，但启动并维持炎症的上游代谢失调仍不明确。本综述探讨线粒体代谢、生物发生及功能障碍如何参与CRS的发病机制。
方法： 截至2025年11月，使用PubMed/MEDLINE、Web of Science和ScienceDirect进行了全面的文献检索。检索词包括“慢性鼻窦炎”、“线粒体”、“氧化应激”、“活性氧”、“炎症”和“上皮屏障”，以及相关关键词和同义词。纳入探讨线粒体参与CRS的实验性、机制性和转化性研究。
结果： 来自多项实验研究的证据表明，线粒体功能障碍与CRS的关键病理过程密切相关。线粒体受到多种CRS相关致病因素的损伤，导致活性氧产生过多、生物发生受损和膜电位破坏。这些线粒体异常放大了上皮炎症、氧化应激和屏障功能障碍，形成线粒体损伤与炎症相互强化的自我传播恶性循环。线粒体功能障碍还促成特征性组织病理学改变，包括上皮损伤、纤毛功能障碍和纤维蛋白沉积。
结论： 线粒体在CRS发病机制中发挥关键作用。因此，靶向这一炎症-氧化应激-线粒体功能障碍的自我放大循环，是打破CRS慢性化的有前景的治疗策略。
英文摘要
BACKGROUND: Chronic rhinosinusitis (CRS) is a common clinical condition characterized by persistent inflammation of the nasal and sinus mucosa. While inflammatory endotypes are well-described, the upstream metabolic dysregulations that initiate and perpetuate inflammation remain poorly defined. This review examines how mitochondrial metabolism, biogenesis, and dysfunction contribute to CRS pathogenesis.
METHODS: A comprehensive literature search was performed up to November 2025 using PubMed/MEDLINE, Web of Science, and ScienceDirect. Search terms included "chronic rhinosinusitis," "mitochondria," "oxidative stress," "reactive oxygen species," "inflammation," and "epithelial barrier," together with related keywords and synonyms. Experimental, mechanistic, and translational studies exploring mitochondrial involvement in CRS were included.
RESULTS: Evidence from multiple experimental studies demonstrates that mitochondrial dysfunction is closely intertwined with key pathological processes in CRS. Mitochondria are damaged by diverse CRS-related pathogenic factors leading to excessive reactive oxygen species production, impaired biogenesis, and disrupted membrane potential. These mitochondrial abnormalities amplify epithelial inflammation, oxidative stress, and barrier dysfunction, creating a self-propagating vicious cycle in which mitochondrial injury and inflammation reinforce each other. Mitochondrial dysfunction also contributes to characteristic histopathological changes, including epithelial damage, ciliary impairment, and fibrin deposition.
CONCLUSIONS: Mitochondria play a pivotal role in CRS pathogenesis. Targeting this self-amplifying cycle of Inflammation-oxidative stress-mitochondrial dysfunction therefore represents a promising therapeutic strategy for breaking the chronicity of CRS.