2025 年第 10 期 第 20 卷

细胞自噬调控长链非编码RNA MALAT1拮抗气道上皮细胞炎症的作用机制研究进展

Research progress on the mechanism of antagonizing airway epithelial cell inflammation by regulating long non-coding RNA MALAT1 by autophagy

作者：赵磊1颜培正2赵晓旻3

英文作者：Zhao Lei1 Yan Peizheng2 Zhao Xiaomin3

单位：1中国人民解放军联勤保障部队第九六六医院药剂科，丹东118000；2山东中医药大学，济南250355；3山东中医药高等专科学校，烟台264100

英文单位：1Department of Pharmacy the 966th Hospital of Joint Logistics Support Force of the Chinese People′s Liberation Army Dandong 118000 China; 2Shandong University of Traditional Chinese Medicine Jinan 250355 China; 3Shandong College of Traditional Chinese Medicine Yantai 264100 China

关键词：气道上皮细胞炎症；细胞自噬；长链非编码RNAMALAT1

英文关键词：Airwayepithelialcellinflammation;Autophagy;Longnon-codingRNAMALAT1

• 摘要：

• 支气管哮喘是以慢性气道炎症为核心病理特征的全球性健康问题，临床表现为喘息、呼吸困难及咳嗽，病理特征包括气道高反应性、可逆性气流受限和临床异质性。气道上皮作为抵御外界刺激的第一道防线，其屏障损伤可导致变应原渗透增加，激活细胞免疫，触发炎症级联反应，加剧气道重塑。研究表明，细胞自噬在调控气道炎症中具有双重作用。长链非编码RNA MALAT1在哮喘患者外周血及肺组织中显著高表达。在哮喘模型中，MALAT1沉默可降低自噬相关蛋白表达，抑制中性粒细胞浸润及炎症反应，改善气道病理特征。未来研究需进一步解析MALAT1在自噬与炎症中的特异性调控网络，并结合高通量技术探索其作为分子标志物或治疗靶点的临床应用潜力，为自噬相关呼吸系统疾病的精准干预奠定理论基础。

• Bronchial asthma is a global health problem with chronic airway inflammation as the core pathological feature. The clinical manifestations are wheezing, dyspnea and cough, and the pathological features include airway hyperresponsiveness, reversible airflow limitation and clinical heterogeneity. Airway epithelium is the first line of defense against external stimuli, and its barrier damage can lead to increased allergen penetration, activate cellular immunity, trigger inflammatory cascades, and exacerbate airway remodeling. Studies have shown that autophagy has a dual role in the regulation of airway inflammation. Long non-coding RNA MALAT1 was significantly up-regulated in peripheral blood and lung tissues of asthmatic patients. In asthma model, silencing MALAT1 can reduce the expression of autophagy-related proteins, inhibit neutrophil infiltration and inflammatory response, and improve airway pathological characteristics. In the future, it is necessary to further analyze the specific regulatory network of MALAT1 in autophagy and inflammation, and to explore its clinical application potential as a molecular marker or therapeutic target combined with high-throughput technology, so as to lay a theoretical foundation for the precise intervention of autophagy-related respiratory diseases.