哺乳动物雷帕霉素靶蛋白在吸烟所致慢性阻塞性肺疾病发病机制中的研究进展

Research progress of mammalian rapamycin target protein in the pathogenesis of chronic obstructive pulmonary diseases caused by smoking

慢性阻塞性肺疾病(COPD)是一种异质性肺部状态,以慢性呼吸道症状(呼吸困难、咳嗽、咳痰、急性加重)为特征,是由气道(支气管炎、细支气管炎)和(或)肺泡(肺气肿)异常所导致的持续性、进行性气流阻塞。当前,COPD的全球发病率和病死率仍居高不下,且认为COPD的发病率与吸烟呈正相关,这可能由于香烟烟雾所引起的气道炎症及异常激活哺乳动物雷帕霉素靶蛋白(mTOR),导致气道上皮细胞生长、增殖、凋亡、自噬,继而促进气道重塑等一系列病理生理特征。目前,吸烟所致的COPD患者仍缺乏有效的治疗方法,探究新的药物靶点开发新药具有重要的临床意义。mTOR是否参与吸烟者COPD的发生和发展,通过何种机制参与,都值得进一步探讨。本文就mTOR在吸烟所致的COPD发病机制中的作用作一综述。

Chronic obstructive pulmonary diseases(COPD)is a heterogeneous lung state,characterized by chronic respiratory symptoms(including dyspnea,cough,expectoration,and acute exacerbation),and is a persistent and usually progressive airflow obstruction caused by airway(such as bronchitis and bronchiolitis)and/or pulmonary alveolar(emphysema)abnormalities.At present,the global incidence and mortality of COPD are still high,and it is believed that the incidence of COPD is positively related to smoking,which may be due to airway inflammation caused by cigarette smoke and abnormal activation of mammalian target of rapamycin(mTOR),leading to a series of pathophysiological characteristics such as airway epithelial cell growth,proliferation,apoptosis,and autophagy,and then promoting airway remodeling.At present,COPD caused by smoking still lacks effective treatment,so it is of great clinical significance to explore new drug targets and to develop new drugs.Whether mTOR participates in the occurrence and development of COPD among smokers and through what mechanism are worth further exploring.This article reviews the role of mTOR in the pathogenesis of COPD induced by smoking.