Chen Daichi, Wu Wanhua, Li Jianing, Huang Xueqin, Chen Su, Zheng TingTing, Huang Gonghua, Ouyang Suidong
Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, The First Dongguan Affiliated Hospital, College of Medical Technology, Guangdong Medical University, Dongguan, 523808, China.
Liaobu Hospital of Dongguan City, Dongguan, 523430, China.
Inflamm Res. 2025 Jan 7;74(1):1. doi: 10.1007/s00011-024-01972-8.
Allergic asthma is a chronic complex airway disease characterized by airway hyperresponsiveness, eosinophilic inflammation, excessive mucus secretion, and airway remodeling, with increasing mortality and incidence globally. The pathogenesis of allergic asthma is influenced by various factors including genetics, environment, and immune responses, making it complex and diverse. Recent studies have found that various cellular functions of mitochondria such as calcium regulation, adenosine triphosphate production, changes in redox potential, and free radical scavenging, are involved in regulating the pathogenesis of asthma. This review explores the involvement of mitochondrial functional changes in the pathogenesis of asthma, and investigate the potential of targeting cellular mitochondria as a therapeutic approach for asthma. Those insights can provide a novel theoretical foundations and treatment strategies for understanding and preventing asthma.
过敏性哮喘是一种慢性复杂性气道疾病，其特征为气道高反应性、嗜酸性粒细胞炎症、黏液分泌过多以及气道重塑，在全球范围内其死亡率和发病率都在上升。过敏性哮喘的发病机制受多种因素影响，包括遗传、环境和免疫反应，这使其变得复杂多样。最近的研究发现，线粒体的各种细胞功能，如钙调节、三磷酸腺苷生成、氧化还原电位变化和自由基清除，都参与调节哮喘的发病机制。本综述探讨线粒体功能变化在哮喘发病机制中的作用，并研究将细胞线粒体作为哮喘治疗靶点的潜力。这些见解可为理解和预防哮喘提供新的理论基础和治疗策略。
