Exploring the interplay between oxidative stress and autophagy in asthma: Pathophysiology and therapeutic potential

Asthma is a chronic respiratory disease, characterized by airway inflammation, hyperresponsiveness, and remodeling. Oxidative stress and autophagy play pivotal roles in asthma pathogenesis. Excessive production of reactive oxygen species (ROS) worsens airway damage and inflammation, and impaired antioxidant defenses in patients with asthma further increase ROS production, leading to tissue damage. Environmental factors, such as allergens and air pollution, and inflammatory cells, such as macrophages and eosinophils, contribute to elevated ROS levels, thereby intensifying the disease. Autophagy, a key mechanism for eliminating damaged organelles and maintaining cellular homeostasis, plays a dual role in asthma. While autophagy activation mitigates oxidative stress, dysregulated or excessive autophagy worsens airway remodeling and inflammation. This review examines the interplay between oxidative stress and autophagy in asthma and discusses emerging therapeutic approaches targeting autophagy to improve disease outcomes.