Abstract
Studies in animal models have demonstrated that the protease ADAMTS7 plays a role in neointima formation after arterial mechanical injury, by facilitating vascular smooth muscle cell (VSMC) migration. Furthermore, recent human genetic studies have revealed an association between DNA polymorphisms at the ADAMTS7 gene locus and risk of coronary artery disease (CAD). Functional studies have shown that a CAD-associated polymorphism in the coding region of the ADAMTS7 gene affects ADAMTS7 maturation and VSMC migration. This editorial highlights these findings and discusses targeted ADAMTS7 inhibition as a possible novel approach to treat CAD.