Chronic obstructive pulmonary disease (COPD) is commonly associated with vascular changes in the pulmonary and systemic circulations. Pulmonary muscular arteries characteristically show intimal hyperplasia, which is produced in part by the proliferation of poorly differentiated smooth muscle cells. The origin of these cells has not been determined. Bone marrow has the capacity to produce and mobilize progenitor cells that may be recruited at sites of vascular damage and contribute to vascular repair through their differentiation into endothelial cells. Nevertheless, under some circumstances bone marrow-derived progenitor cells may migrate into the intima and differentiate into smooth muscle cells. Local factors and cell-to-cell contact are critical in determining the fate of progenitor cells in the vessel wall. Studies assessing the number of circulating bone marrow-derived vascular progenitor cells indicate that COPD is characterized by a reduction in circulating hemopoietic and vascular progenitors. The mechanisms of this reduction have not been elucidated. It has been suggested that this process may lead to reduced vascular repair capacity and increase the risk of cardiovascular complications, which are associated with significant morbidity and mortality in COPD. Further investigation in this field and elucidation of the underlying mechanisms will contribute to a better management of this major complication of COPD.