Reactive oxygen species (ROS) play a critical role in cardiovascular diseases such as hyperlipidemia, diabetes, hypertension, ischemic heart disease, and chronic heart failure. ROS are produced by inflammatory and vascular cells, including endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts, and have diverse effects on cell function, including growth, apoptosis, migration, and inflammation. ROS can regulate vascular function and contribute to vascular disease. Superoxide (O₂⁻) is a major ROS in the vasculature, generated by enzymes like NAD(P)H oxidases and xanthine oxidase. O₂⁻ can generate other ROS, such as peroxynitrite and hydrogen peroxide (H₂O₂), which can further contribute to oxidative stress. ROS are involved in various vascular processes, including endothelial dysfunction, apoptosis, adhesion molecule expression, angiogenesis, and vascular smooth muscle cell (VSMC) growth and migration. ROS also regulate matrix remodeling and inflammatory gene expression, such as NF-κB activation, which is central to atherosclerosis. In hypertension, ROS contribute to vascular remodeling and increased oxidative stress. In diabetes, hyperglycemia and free fatty acids increase ROS production, leading to vascular dysfunction. ROS are also involved in restenosis after angioplasty. Despite their role in disease, antioxidant therapies have not consistently shown clinical benefits, possibly due to the complexity of ROS regulation and the need for more effective antioxidants. Understanding the role of ROS in vascular disease is essential for developing targeted therapies.Reactive oxygen species (ROS) play a critical role in cardiovascular diseases such as hyperlipidemia, diabetes, hypertension, ischemic heart disease, and chronic heart failure. ROS are produced by inflammatory and vascular cells, including endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts, and have diverse effects on cell function, including growth, apoptosis, migration, and inflammation. ROS can regulate vascular function and contribute to vascular disease. Superoxide (O₂⁻) is a major ROS in the vasculature, generated by enzymes like NAD(P)H oxidases and xanthine oxidase. O₂⁻ can generate other ROS, such as peroxynitrite and hydrogen peroxide (H₂O₂), which can further contribute to oxidative stress. ROS are involved in various vascular processes, including endothelial dysfunction, apoptosis, adhesion molecule expression, angiogenesis, and vascular smooth muscle cell (VSMC) growth and migration. ROS also regulate matrix remodeling and inflammatory gene expression, such as NF-κB activation, which is central to atherosclerosis. In hypertension, ROS contribute to vascular remodeling and increased oxidative stress. In diabetes, hyperglycemia and free fatty acids increase ROS production, leading to vascular dysfunction. ROS are also involved in restenosis after angioplasty. Despite their role in disease, antioxidant therapies have not consistently shown clinical benefits, possibly due to the complexity of ROS regulation and the need for more effective antioxidants. Understanding the role of ROS in vascular disease is essential for developing targeted therapies.