Platelets are essential mediators of inflammation and thrombosis. Chronic obstructive pulmonary disease (COPD) is a heterogeneous multisystem disease, causing significant morbidity and mortality worldwide. Recent evidence suggests that the lung is an important organ for platelet biogenesis. Cigarette smoking has been shown to induce platelet aggregation and decrease the capacity of mitochondrial electron transport system in platelets. Preclinical and clinical studies have suggested that platelets may contribute to the development of COPD through the breakdown of lung elastin by platelet factor 4, platelet activation and formation of platelet aggregates, and modulation of hypoxia signaling pathways. Recent large population studies have produced encouraging results indicating a potential role for aspirin in preventing exacerbations and delaying disease progression in patients with COPD. This review summarizes the information about the lung as an organ for platelet production, pathophysiological functions of platelets and platelet mediators in the development of COPD, and the most updated evidence on the utility of aspirin in patients with COPD.

血小板是炎症和血栓形成的重要介质。慢性阻塞性肺疾病（COPD）是一种异质性多系统疾病，在世界范围内引起大量发病和死亡。最近的证据表明，肺是血小板生物发生的重要器官。吸烟已显示可诱导血小板聚集并降低血小板中线粒体电子转运系统的能力。临床前和临床研究表明，血小板可能通过血小板因子4分解肺弹性蛋白而促进COPD的发展，血小板活化和血小板聚集物的形成以及缺氧信号通路的调节。最近的大量人群研究产生了令人鼓舞的结果，表明阿司匹林在预防COPD患者病情恶化和延缓疾病进展方面具有潜在作用。这篇综述总结了有关肺作为血小板产生器官的信息，血小板和血小板介质在COPD发展中的病理生理功能，以及有关阿司匹林在COPD患者中的效用的最新证据。