elastin and Mitochondrial-Diseases

Platelets are essential mediators of inflammation and thrombosis. Chronic obstructive pulmonary disease (COPD) is a heterogeneous multisystem disease, causing significant morbidity and mortality worldwide. Recent evidence suggests that the lung is an important organ for platelet biogenesis. Cigarette smoking has been shown to induce platelet aggregation and decrease the capacity of mitochondrial electron transport system in platelets. Preclinical and clinical studies have suggested that platelets may contribute to the development of COPD through the breakdown of lung elastin by platelet factor 4, platelet activation and formation of platelet aggregates, and modulation of hypoxia signaling pathways. Recent large population studies have produced encouraging results indicating a potential role for aspirin in preventing exacerbations and delaying disease progression in patients with COPD. This review summarizes the information about the lung as an organ for platelet production, pathophysiological functions of platelets and platelet mediators in the development of COPD, and the most updated evidence on the utility of aspirin in patients with COPD.

Topics: Aspirin; Blood Platelets; Disease Progression; Elastin; Electron Transport; Humans; Inflammation; Lung; Megakaryocytes; Mitochondria; Mitochondrial Diseases; Platelet Activation; Platelet Aggregation; Platelet Aggregation Inhibitors; Platelet Factor 4; Pulmonary Disease, Chronic Obstructive; Smoking; Thrombosis