Oxidative stress and inflammation trigger atherothrombosis. The scheme illustrates the activation of immune cells and recruitment to vascular tissues by classical cardiovascular risk factors, leading to the activation of secondary vascular ROS sources such as NADPH oxidase (Nox1, Nox2, and Nox4), xanthine oxidase (conversion of the dehydrogenase (XDH) to the oxidase (XO) form), mitochondria (via mitochondrial redox switches (RS)), and uncoupled eNOS (oxidative depletion of tetrahydrobiopterin (BH4) and other redox switches), all of which contribute to vascular dysfunction, progression of atherosclerosis, and thrombus formation. Adhesion molecules and chemokines (VCAM-1, ICAM-1, E-selectin, and MCP-1) play an important role for leukocyte recruitment to vascular tissues leading to the secondary damage. Endogenous antioxidant defense proteins (e.g., superoxide dismutases, glutathione peroxidases, heme oxygenase-1, and AMP-activated protein kinase) interfere with oxidative damage and redox-dependent inflammatory processes. Also, modern antidiabetic cardiovascular drugs (e.g., SGLT2 inhibitors, DPP-4 inhibitors, and GLP-1 analogs) suppress inflammatory and adverse redox pathways and thereby decrease cardiovascular risk. Modified from Steven et al. [8
]. Open access article distributed under the Creative Commons Attribution License (CC BY 4.0).