To discuss crucial cues (chemokines, adhesion molecules and pharmacological means) that guide and control the context-specific mobilization, recruitment and fate of circulating progenitor cells in arterial repair and plaque stability. The mobilization and recruitment of bone marrow derived or resident progenitor cells giving rise to smooth muscle cells have been implicated in accelerated forms of primary plaque formation and neointimal hyperplasia after arterial injury. By contrast, convincing evidence has emerged that the arterial homing of endothelial progenitor cells contributes to endothelial recovery and thereby limits neointimal growth after endothelial denudation. In the chronic context of primary atherosclerosis, plaque progression and destabilization, a more complex picture has become apparent. Clinically, the number and function of endothelial progenitor cells have been linked with an improved endothelial function or regeneration and have been frequently inversely correlated with cardiovascular risk (factors). In animal models, however, the injection of bone marrow cells or endothelial progenitor cells, as well as the application of stem-cell mobilizing factors, have been associated with an exacerbation of atherosclerosis and unstable plaque phenotype, whereas the contribution of smooth muscle progenitors to primary atherosclerosis appears to be more confined to supporting plaque stability. Considering the balance between distinct circulating vascular progenitor cells and identifying mechanisms for selective control of their mobilization and homing appears crucial to improve prediction and to directly modulate endogenous vascular remodeling processes.