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Bronchopulmonary dysplasia (BPD), also known as neonatal chronic lung disease, is a multifactorial disease and its pathogenesis starts even before birth. Animal models of BPD and the study of infants with BPD suggest that impaired lung vascular development leads to the failure of alveolar development and strategies that promote vascular development result in improved aralveolization of the lung. Since 1997 when Asahara identified endothelial cell progenitors (EPCs) as blood cells having the ability to contribute to postnatal vasculogenesis, several studies have attempted to elucidate the role of EPCs in neonatal lung development and lung injury and repair. This review outlines the progress in defining early EPCs (believed to be of hematopoietic origin) and late EPCs or true EPCs (believed to be of endothelial origin) through the use of cell culture assays and flow cytometric characterization. Both animal and human studies have attempted to correlate the frequency of these specific populations with susceptibility to BPD. Animal studies use hyperoxia or endotoxininduced lung injury as a model of BPD. Human studies use frequencies of specific cell populations as a prognostic index of BPD. Conflicting outcomes are likely the result of a lack of consistent definitions. Recently, there is increasing evidence that blood and bone marrow-derived stem cells exert a beneficial effect in models of chronic lung injury, not so much by engraftment and differentiation, but by a paracrine effect on the existing lung progenitor cells.