Kailin Zhou, Qianmei Wen, Yujie Zuo, Ge Bai, Ruiting Sun

State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, People’s Republic of China

Correspondence: Ruiting Sun, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, No. 151 Yanjiang Road, Yuexiu District, Guangzhou, 510120, People’s Republic of China, Email Dr.srt@hotmail.com

Abstract: The pathological alterations in COPD cells represent adaptive responses to COPD lesions, focusing on three primary pathological changes: abnormal repair and tissue remodeling, protease-antiprotease imbalance, and inflammatory amplification alongside immune disorder. These alterations ultimately result in a detrimental cycle of lung parenchymal destruction and airway structural remodeling. COPD manifests with diverse pathological phenotypes, pronounced heterogeneity, and a convoluted evolution process. However the role of pathological changes and mechanisms in pathological cells, as well as cellular senescence, metabolic reprogramming, and intercellular interaction networks in COPD, remains unclear. This review comprehensively encapsulates the most recent research advancements regarding the principal pathological cells in COPD, encompassing airway epithelial cells, fibroblasts, endothelial cells, and immune inflammatory cells. Elucidated the pathological alterations of these cells in relation to COPD, their influence on disease progression, and their clinical implications. Furthermore, Exosome-mediated miRNA transfer exacerbates inflammation and fibrosis, suggesting novel therapeutic targets. In summary, our work aims to provide a basic reference for research into the pathogenic mechanisms of this disease.

Keywords: chronic obstructive pulmonary disease, airway epithelial cells, fibroblasts, endothelial cells, immune inflammatory cells, extracellular vesicles, miRNA, NETosis, cellular senescence