The Role of Mitochondria and Oxidative/Antioxidative Imbalance in Pathobiology of Chronic Obstructive Pulmonary Disease.

摘要: Chronic obstructive pulmonary disease (COPD) is a common preventable and treatable disease, characterized by persistent airflow limitation that usually progressive associated with an enhanced chronic inflammatory response in the airways lung to noxious particles or gases. The major risk factor of COPD, which has been proven many studies, exposure cigarette smoke. However, it 15–20% all smokers who develop COPD. This why we should recognize pathobiology COPD as involving complex interaction between several factors, including genetic vulnerability. Oxidant-antioxidant imbalance recognized one significant factors pathogenesis. Numerous exogenous endogenous sources ROS are present One mitochondria. Although leakage electrons from electron transport chain forming effect physiological functioning mitochondria, there various intra- extracellular may increase this amount significantly contribute oxidative-antioxidative imbalance. With coexistence impaired antioxidant defence, these issues lead oxidative carbonyl stress. Both states play role account for development comorbidities disease.