Molecular mechanisms and cellular process in signal transduction pathway related to air pollutants in obstructive lung diseases: A mini-review

Exposure to air pollutants such as PM10, PM2.5, PM0.1, O3, CO, NO2, and SO2, and biological pollutants are important factors causing the evolution and furtherance of obstructive lung diseases (OLD), including asthma and chronic obstructive pulmonary disease (COPD). Asthma is the most frequent chronic inflammatory airway disease, characterized by breathlessness, wheezing, chest tightness, and cough, together with the presence of exaggerated expiratory airflow fluctuation that varies over time. COPD is a heterogeneous lung condition characterized by chronic respiratory symptoms such as dyspnea, cough, expectoration, and/or exacerbations due to abnormalities of the airways and/or alveoli that cause persistent, often progressive, airflow obstruction. Understanding the molecular mechanisms and cellular processes based on the development of OLD on exposure to air pollutants will provide insights into the solution of pathogenesis, prevention, and treatment of these conditions. The molecular mechanisms and cellular process involved in signal transduction pathway plays a role in the binding of extracellular signaling molecules and ligands to receptors placed on the cell surface or on the inner side cell that trigger inflammation that occurs, especially when something important enters the cell to bring into a cascade response. This binding then alters the cell metabolism, shape, and gene expression in the airway. This review aimed to reveal the effect of air pollutants on the molecular mechanisms and cellular processes involved in the signal transduction pathways in OLD.