Li Z, Wu J, Zhang X, et al. - In this study, using in vitro, ex vivo and in vivomodels, researchers examined the role of the cell division cycle 42 (CDC42) in vascular calcification (prevalent in individuals with chronic kidney disease (CKD) and a significant risk factor of cardiovascular disease). A notable rise during vascular calcification, in the expression of CDC42 both in rat vascular smooth muscle cells (VSMCs) and in calcified arteries, was noted. Via alizarin red staining and calcium content assay, it was exhibited that adenovirus-mediated CDC42 overexpression in the presence of the calcifying medium, resulted in an apparent VSMC calcification, along with up-regulation of bone-related molecules including runt-related transcription factor 2 and bone morphogenetic protein 2. On the contrary, in vitro and aortic rings ex vivo, inhibition of CDC42 by ML141 significantly obstructed calcification of VSMCs. Furthermore, in rats with CKD, ML141 considerably attenuated vascular calcification. Besides, the pharmacological restraint of the AKT signal was explicated to block CDC42-induced VSMC calcification. Thus, these findings exhibited for the first time that via a mechanism involving AKT signaling, CDC42 adds to vascular calcification, which revealed a new function of CDC42 in regulating vascular calcification. Moreover, in context to CKD, for the treatment of vascular calcification, this could give a potential therapeutic target.