Inflammatory cytokines play a critical role in vascular dysfunction and disease. These cytokines, produced by various cells including macrophages, T cells, and vascular cells, interact with cell receptors to activate signaling pathways such as JAK-STAT, NF-κB, and Smad, leading to inflammation, cell adhesion, permeability, and apoptosis. Cytokines also affect mitochondrial function, increasing reactive oxygen species (ROS) production, which can damage vascular cells. They influence the production of vasodilators and vasoconstrictors, modify the extracellular matrix (ECM), and affect vascular smooth muscle cells (VSMCs) by activating pathways like Ca²⁺, protein kinase C, Rho-kinase, and MAPK. Persistent cytokine elevation is linked to vascular diseases such as atherosclerosis, abdominal aortic aneurysm, varicose veins, and hypertension. Cytokine antagonists may offer new therapeutic approaches for inflammatory vascular disease. Cytokines are classified into various types, including TNF, interleukins, chemokines, and others, with distinct sources and signaling mechanisms. They affect endothelial cells (ECs), VSMCs, and ECM, contributing to vascular dysfunction. Cytokines can induce vascular cell growth, migration, and apoptosis, and influence vascular tone, signaling pathways, and ECM composition. They also affect EC function, NO production, and vascular permeability. Cytokines like TNF-α and IL-6 promote VSMC proliferation and migration, contributing to atherogenesis. Cytokines can also enhance ECM degradation via matrix metalloproteinases (MMPs). Vascular factors can influence cytokine production, and cytokines can regulate vascular factors. Inflammatory cytokines are involved in various vascular diseases, including atherosclerosis, hypertension, and preeclampsia. Understanding cytokine mechanisms is crucial for developing new therapies for vascular diseases.Inflammatory cytokines play a critical role in vascular dysfunction and disease. These cytokines, produced by various cells including macrophages, T cells, and vascular cells, interact with cell receptors to activate signaling pathways such as JAK-STAT, NF-κB, and Smad, leading to inflammation, cell adhesion, permeability, and apoptosis. Cytokines also affect mitochondrial function, increasing reactive oxygen species (ROS) production, which can damage vascular cells. They influence the production of vasodilators and vasoconstrictors, modify the extracellular matrix (ECM), and affect vascular smooth muscle cells (VSMCs) by activating pathways like Ca²⁺, protein kinase C, Rho-kinase, and MAPK. Persistent cytokine elevation is linked to vascular diseases such as atherosclerosis, abdominal aortic aneurysm, varicose veins, and hypertension. Cytokine antagonists may offer new therapeutic approaches for inflammatory vascular disease. Cytokines are classified into various types, including TNF, interleukins, chemokines, and others, with distinct sources and signaling mechanisms. They affect endothelial cells (ECs), VSMCs, and ECM, contributing to vascular dysfunction. Cytokines can induce vascular cell growth, migration, and apoptosis, and influence vascular tone, signaling pathways, and ECM composition. They also affect EC function, NO production, and vascular permeability. Cytokines like TNF-α and IL-6 promote VSMC proliferation and migration, contributing to atherogenesis. Cytokines can also enhance ECM degradation via matrix metalloproteinases (MMPs). Vascular factors can influence cytokine production, and cytokines can regulate vascular factors. Inflammatory cytokines are involved in various vascular diseases, including atherosclerosis, hypertension, and preeclampsia. Understanding cytokine mechanisms is crucial for developing new therapies for vascular diseases.