Oxidative stress, a state of excessive reactive oxygen species (ROS) activity, has been implicated in the pathogenesis of cardiovascular disease, including atherosclerosis, hypertension, and restenosis. Recently we have identified several SOXFs (Secreted OXidative stress-induced Factors) from vascular smooth muscle cells (VSMC). Our studies have demonstrated that SOXF function as redox mediators to regulate growth of VSMC, inflammation and apoptosis of endothelial cells, and are involved in the processes of vascular lesion formation after vascular injury and in apolipoprotein E deficient (ApoE-/-) mice. Understanding the mechanisms by which ROS stimulate secretion of SOXF and the role of SOXF in vascular cells should provide important insight into the cellular response to oxidative stress and new therapeutic targets for vascular diseases.