Pathogenic Cell in COPD: Mechanisms of Airway Remodeling, Immune Dysregulation, and Therapeutic Implications

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

Graphical abstract

Figure 1

Pathological changes in airway epithelial cells in COPD.

Figure 2

Pathological intercellular communication pathways mediated by extracellular vesicles in COPD.