Vascular calcification is associated with increased cardiovascular morbidity and mortality and has long been associated with advanced atherosclerotic lesions. While vascular calcification is considered a surrogate marker for atherosclerosis, the mechanisms that link the two are poorly understood. The consensus of recent research is that active regulatory processes govern vascular calcification, and much focus has been placed on elucidating the phenomenon of atherosclerotic calcification. Building upon extensive in vitro work and the previous development of atherosclerotic murine models, several groups have developed murine models of atherosclerotic calcification. From imposing chronic renal failure to developing double-knockout mice, this recent work has provided insight into the pathophysiology of mineralized matrix formation in atherosclerotic lesions, as well as development of potential therapies to prevent or inhibit progression of calcified plaque. The aim is to briefly review current understanding of the molecular basis for atherosclerotic calcification and to discuss some murine models that may be useful in advancing knowledge of its mechanisms.