It is well known that atherosclerosis prevails in elderly populations as ageing acts as a recognized risk factor for this disease. Although the pathogenic factors leading to atherosclerosis are highly heterogeneous, traditionally speaking, the causative risk factors include hyperlipidemia, hypertension, diabetes mellitus and smoking, which can damage to endothelial function, and subsequently promote lipid penetration and inflammatory cell infiltration. Damaged endothelial cells (ECs) may be replaced by neighboring cell division, while damaged smooth muscle cells (SMCs) may be replaced by medial SMCs emigrating into the intima during atherogenesis. However, this standpoint is challenged by recent findings that vascular progenitor/stem cells (VPCs) may contribute to atherogenesis and post-angioplasty restenosis. VPCs are a group of primitive cells that have the potential to produce mature, functional cells in the vascular wall. VPCs residing in bone marrow, vascular wall or circulating in the peripheral blood may be stimulated by a variety of pathogenic factors. These stem cells then participate in regeneration, repair and remodeling of the injured arterial wall. This new concept may bring about a great breakthrough in understanding the pathogenesis of atherosclerosis and develop novel therapeutic strategies for coronary heart disease. This article will mainly review the role of VPCs in atherogenesis, thus providing a novel understanding about the pathophysiology of atherosclerosis.