A comprehensive review of ferroptosis in environmental pollutants-induced chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a common chronic lung disease that impacts hundreds of millions of individuals worldwide. It is principally characterized by irreversible and progressive airflow limitation. Environmental pollutants, including cigarette smoke, air pollution, occupational pollutants, remain predominant risk factors for COPD and play remarkable roles in COPD progression. Despite the availability of treatments to alleviate symptoms of COPD, it continues to exert a serious health and socioeconomic burden. Ferroptosis, a unique form of iron-dependent cell death distinguished by lipid peroxidation, is implicated in various diseases. Recent studies, utilizing COPD patients samples, animal models, and Gene Expression Omnibus (GEO) database, have revealed that ferroptosis is involved in pathogenesis of COPD. Inhibiting ferroptosis signaling pathways halts the progression of COPD. This review consolidates current insights into the mechanisms of ferroptosis in environmental pollutants-induced COPD, which might offer a novel therapeutic strategy for COPD.