Abstract
Chronic obstructive pulmonary disease (COPD) is a highly prevalent airway disorder. However, the mechanisms of the pathogenesis of COPD have not been completely elucidated to date. Transforming growth factor (TGF)-β is a pleiotropic, multifunctional cytokine participating in cell differentiation, apoptosis, survival and proliferation. TGF-β is involved in many diseases, including carcinogenesis and fibrosis. Although the most important risk factor for COPD is cigarette smoking, only 10–15% of all smokers develop the disease. This finding raises suspicion that some host or genetic factors may be involved in the pathogenesis of the disease. Thus, special attention has recently been focused on the role in COPD of TGF-β, which is active in inflammation of the airways and particularly in lung remodeling. TGF-β induces chemotaxis of mast cells and macrophages, regulates cell apoptosis and influences the protease/antiprotease balance inhibiting matrix metalloproteinase-9. TGF-β is heavily involved in repair processes. It is one of the inducers of angiogenesis, plays a role in maintaining the integrity of the pulmonary vasculature and is active in pulmonary tissue fibrosis and the development of lung emphysema. A lot of attention has been concentrated on a possible association between TGF-β1 gene polymorphism and the risk of COPD. There have been a limited number of studies on this topic, and conflicting results have been obtained. TGF-β is also considered a potential therapeutic target in COPD. Despite many attempts, these novel strategies remain in a pre-clinical phase of development and require further investigation.