Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterised by a progressive airflow limitation. Airway smooth muscle (ASM) dysfunction, such as cell hyperproliferation and increased extracellular matrix deposition, contributes to airway remodelling, an important pathological feature of COPD. There is also evidence of defective mitochondria in the lungs and in cultured ASM cells (ASMCs) from patients with COPD. Cigarette smoke (CS), the main cause of COPD, induces cellular and mitochondrial dysfunction, but only a proportion of smokers develop COPD. Homeostatic mechanisms that prevent sustained damage in response to CS may be impaired in COPD. Transfer of mitochondria from stem cells to structural cells in the lung protects the latter from stress-induced mitochondrial dysfunction. In this study, I hypothesised that mitochondrial transfer between ASMCs is a homeostatic mechanism that preserves mitochondrial function, and that it is impaired in COPD leading to sustained mitochondrial dysfunction in response to stress. I show that CS leads to persistent mitochondrial damage in ASMCs, an effect that is more pronounced in cells from COPD patients. However, it remains unclear whether this drives pathogenic ASM phenotypes. I demonstrate that ASMCs, from both healthy and COPD patients, are capable of exchanging mitochondria, a process that occurs, at least partly, via extracellular vesicles. Mitochondrial transfer is induced by exposure to CS, suggesting it is a stress response mechanism. Contrary to my hypothesis, the results of this study indicate that mitochondrial transfer may not be impaired in COPD. However, irrespective of disease status, this process is associated with an up-regulation of mitochondrial respiration and a reduction in cell proliferation. Therefore, mitochondrial transfer between ASMCs may be exploited as an endogenous protective mechanism to reverse mitochondrial and cellular dysfunction in the lungs.