ABSTRACT
Bronchial asthma is a chronic inflammatory disease of the airways, which is characterized by airway hyperresponsiveness(AHR), eosinophilia, elevated IgE, goblet cell metaplasia, airway remodeling and so on.Changes in airway epithelial structure and function are prominent features of asthma.Asthma airway epithelium has abnormal sensitivity to oxidative damage and apoptosis, and is more susceptible to reactive oxygen species(ROS)produced by infiltrating inflammatory cells.The effects of ROS accumulation and oxidative stress are the key links in the pathogenesis of asthma.Oxidants such as ROS can interfere with the structure of epithelial cells and cause tracheal remodeling.Conversely, tracheal remodeling can release inflammatory mediators and aggravate asthma.The main function of mitochondria is oxidative phosphorylation to synthesize ATP, and it is also an important source of ROS.Mitochondrial dysfunction includes energy metabolism conversion dysfunction, mitochondrial biological dysfunction, mitochondrial autophagy and kinetic abnormalities, and mitochondrial-dependent signaling pathway disorders.Mitochondrial dysfunction and cellular hypoxia play an extremely important role in the occurrence and development of bronchial asthma.This article reviews the changes in mitochondrial function of airway epithelial cells in asthma airways in recent years, in order to provide theoretical basis for mitochondria-targeted asthma treatment.