COPD is defined as an irreversible expiratory airflow limitation, which is caused by various degrees of the following two main features: First, small airway disease (SAD), which includes airway inflammation and remodelling, and second, emphysema, which is characterised by airspace enlargement. The major risk factor for COPD is cigarette smoke exposure; however, the molecular mechanisms linking smoke to different COPD features on the cellular level remain elusive. The transforming growth factor (TGF)-β superfamily constitutes more than 40 members, which are essential during organ development, a process often recapitulated in chronic diseases. Emerging interest in the role of TGF-β in the pathogenesis of COPD has recently evolved, particularly since genetic studies have demonstrated an association of gene polymorphisms of the TGF-β superfamily with COPD. In addition, increased expression of TGF-β1 in COPD lungs and primary cells, such as epithelial cells, macrophages, or fibroblasts isolated from COPD specimens, was reported, suggesting an impact of TGF-β signalling on the development and progression of COPD. Thus, targeted interventions of TGF-β signalling may represent a suitable therapeutic option in COPD. In this review, we will summarise the current understanding of the impact of TGF-β in COPD pathogenesis. The review is separated into five chapters: 1) an introduction to COPD, 2) an introduction to TGF-β signalling, 3) a summary of TGF-β gene polymorphisms in COPD, 4) a summary of TGF-β signalling in small airway disease, and 5) a summary of TGF-β signalling in emphysema.