Medin, a 50-residue cleavage polypeptide of milk fat globule protein epidermal growth factor 8 (MFG-E8), has been deemed to play key roles in the pathogenesis of many cardiovascular diseases, including aortic amyloidosis, hypertension, atherosclerosis, aortic dissection, heart failure, and coronary artery disease. The interactions between medin and vascular cells, such as endothelial cells in intima, vascular smooth muscle cells in media, and fibroblasts in adventitia, are considered to be involved in the pathophysiological processes of the vascular remodelling that underlies cardiovascular diseases. Recent evidence has indicated that medin could also act as a scaffold to facilitate the depositions of other types of amyloid proteins, thereby inducing cardiovascular injuries.