The use of animal models in the study of arteriosclerosis is essential for better understanding of the pathogenesis, improvement in diagnosis, prevention and therapy of the diseases in humans. Recently numerous investigators started to use mouse models to study the pathogenesis of cardiovascular diseases. This species is particularly valuable which is believed to have some advantages over other strains, because of the availability of well-defined genetic systems of transgenic and knockout mice. Concomitantly, we have established the mouse models for vein grafts and transplant arteriosclerosis. By using these models, we have learned much knowledge concerning the pathogenesis of the disease and possible therapeutic intervention has been gained. One of most important findings is that proteins or molecules influencing apoptosis, inflammation or proliferation of vascular smooth muscle cells or endothelial cells, have been found to enhance or inhibit neointimal lesion formation in knockout or mutant mice in these models. Furthermore, the findings on the origins of endothelial and smooth muscle cells in lesions of vein graft and transplant atherosclerosis provided basic information that have challenged the traditional hypothesies. Using these models, it has also been demonstrated that stem cells identified in blood and bone marrow as well as the vasculature contribute to the atherosclerotic lesion formation, supporting the importance of murine models of vessel grafts in understanding the mechanisms of the vascular diseases. The present review updates the progress of the research in this field, by summarizing data of using mouse models of vessel grafts, and provides a perspective analysis on the future directions.