The vascular inflammatory response involves complex interactions between inflammatory cells (neutrophils, lymphocytes, monocytes, macrophages), endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM). Vascular injury triggers increased expression of adhesion molecules by ECs and the recruitment of inflammatory cells, growth factors, and cytokines, leading to altered ECs, VSMCs, and ECM functions. Cytokines, including tumor necrosis factors, interleukins, lymphokines, monokines, interferons, colony-stimulating factors, and transforming growth factors, are produced by various immune and vascular cells. They interact with specific receptors on target cells, activating signaling pathways such as JAK-STAT, NF-κB, and Smad, which modulate cell adhesion, permeability, and apoptosis. Cytokines also increase reactive oxygen species (ROS) production and modify the production and activity of vasodilatory and vasoconstrictive mediators. In persistent high levels, cytokines contribute to vascular dysfunction and diseases such as atherosclerosis, abdominal aortic aneurysm, varicose veins, and hypertension. Genetic and pharmacological approaches to reduce cytokine production or their effects using antagonists offer new therapeutic strategies for inflammatory vascular diseases.The vascular inflammatory response involves complex interactions between inflammatory cells (neutrophils, lymphocytes, monocytes, macrophages), endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM). Vascular injury triggers increased expression of adhesion molecules by ECs and the recruitment of inflammatory cells, growth factors, and cytokines, leading to altered ECs, VSMCs, and ECM functions. Cytokines, including tumor necrosis factors, interleukins, lymphokines, monokines, interferons, colony-stimulating factors, and transforming growth factors, are produced by various immune and vascular cells. They interact with specific receptors on target cells, activating signaling pathways such as JAK-STAT, NF-κB, and Smad, which modulate cell adhesion, permeability, and apoptosis. Cytokines also increase reactive oxygen species (ROS) production and modify the production and activity of vasodilatory and vasoconstrictive mediators. In persistent high levels, cytokines contribute to vascular dysfunction and diseases such as atherosclerosis, abdominal aortic aneurysm, varicose veins, and hypertension. Genetic and pharmacological approaches to reduce cytokine production or their effects using antagonists offer new therapeutic strategies for inflammatory vascular diseases.