Vascular calcification is a major contributing factor of morbidity and mortality in patients with atherosclerosis, chronic kidney disease and diabetes. Vascular calcification is an active, cell-regulated process of matrix mineral metabolism resulting in the deposition of calcium phosphate in the arterial wall which has many similarities to bone formation. This phenomenon includes the dedifferentiation or transform of vascular smooth muscle cells (VSMCs) to a phenotypic switch with osteogenic characteristics in the setting of chronic kidney disease, diabetes, aging or inflammation. Once the osteogenic phenotype is induced, cells of the vascular wall increase levels of osteogenic markers including runt-related transcription factor 2 (Runx2), Msx2 or osterix, while loss endogenous inhibitors of mineralization, such as matrix γ-carboxyglutamic acidprotein (MGP) and fetuin. To induce vascular calcification, vascular smooth muscle cells (Human, Mice, or Rat aorta smooth muscle cell, VSMC) are cultured with calcification medium containing inorganic phosphate or β-Glyccerophosphate. Calcification medium-induced VSMC calcification is confirmed by morphological changes and increased intracellular of calcium content using von kossa stain or Alizarin Red S stain. The expression of osteogenic markers including BMP2, Runx2, Msx2 can be evaluated. Animal lacking gene that regulate bone formation including MGP, OPG and, smad6 gene product develop varying extents of arterial calcification. Atherogenic high-fat diet in murine knockout models of genes (ApoE or LDL), nephrectomy or Vitamin D toxicity animal model also have used commonly for vascular calcification. In this talk, I will discuss the current knowledge about pathogenesis of vascular calcification and reviews the new insight into the more physiologic vascular calcification models.