Molecular Mechanisms of Programmed Cell Death Pathways in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) represents a prevalent respiratory ailment, which is distinguished by enduring airflow obstruction and a tendency to progress over time. Over 400 million people globally are currently impacted. Alveolar epithelial cells, airway epithelial cells, and important inflammatory cell populations are all actively involved in the pathological development of COPD. These cells' interactions have wide-ranging physiological effects on the body, such as aggravating lung damage and inducing inflammation, which are the pathogenic causes of COPD. In the present review, numerous programmed cell death (PCD) modes are addressed with a focus on molecular mechanisms and crosstalk of seven PCD processes-apoptosis, necroptosis, ferroptosis, autophagy, pyroptosis, cuproptosis, and disulfidptosis-in COPD pathogenesis and initiation. It also refers to clinical treatment strategies for the acute and stable phases of COPD based on PCD regulation. From the cellular perspective, we may have a more exact understanding of disease phenotypes; demystification of cell-type-specific mechanisms is aimed at providing theoretical guidance for further probing of COPD's molecular pathology and development of novel therapeutic strategies against PCD.