Role of oxidative stress induced by cigarette smoke in the pathogenicity of chronic obstructive pulmonary disease

Abstract

Cigarette smoke (CS) exposes lungs to oxidative stress and inflammation and is a major risk factor for the development of chronic obstructive pulmonary disease (COPD). COPD is a complex lung disease characterized by chronic inflammation with limited airflow and chronic bronchitis associated with mucus hypersecretion, thickened small airway walls, and emphysema. CS-induced oxidative stress is responsible for altered cellular metabolism, including increased infiltrating immune cells, pro-inflammatory cytokine production, protease-antiprotease imbalance, lipid peroxidation, apoptosis, upregulation of unfolded protein response (UPR), and protein misfolding. This chapter reviews the current knowledge on different mechanisms through which both direct and secondhand CS-induced oxidative stress in lungs plays a significant role in the pathogenesis of COPD. Despite the presence of considerable reports recognizing the harmful effects of CS-generated oxidative stress, effective treatment for COPD is lacking. Extensive research on the immune and pathogenetic mechanisms of COPD will help in developing new treatment strategies. Clinical trials leveraging multiple antioxidants, anti-inflammatory processes, and UPR inhibitors are urgently needed to advance COPD therapies.