Chronic obstructive pulmonary disease (COPD) is one of the leading global causes of
morbidity and mortality. A hallmark of COPD is progressive airflow obstruction primarily caused by
cigarette smoke (CS). CS exposure causes an imbalance favoring pro- over antioxidants (oxidative
stress), leading to transcription factor activation and increased expression of inflammatory mediators
and proteases. Different cell types, including macrophages, epithelial cells, neutrophils, and T lymphocytes, contribute to COPD pathophysiology. Alteration in cell functions results in the generation
of an oxidative and inflammatory microenvironment, which contributes to disease progression. Current treatments include inhaled corticosteroids and bronchodilator therapy. However, these therapies
do not effectively halt disease progression. Due to the complexity of its pathophysiology, and the
risk of exacerbating symptoms with existing therapies, other specific and effective treatment options
are required. Therapies directly or indirectly targeting the oxidative imbalance may be promising
alternatives. This review briefly discusses COPD pathophysiology, and provides an update on the
development and clinical testing of novel COPD treatments