The development of atherosclerotic lesions leading to myocardial infarction (MI) or stroke encompasses a cascade of cellular and molecular events that can well be characterized as a chronic immune-mediated inflammation occurring preferentially in the biologic surrounding of the so called metabolic syndrome. Adipokines, chemokines, cytokines, and their receptors are critically involved in the initiation and perpetuation of atherosclerosis, and they play important roles at all levels in the pathogenesis of this disease. Metabolic risk profiles associated with sedentary lifestyle, obesity, especially intra-abdominal fat accumulation, insulin resistance, and dyslipidemia pave the way for a chronic, immunemediated vascular inflammation around vascular lipid deposits. In the present article, the impact of adiponectin, monocyte and T-cell associated cytokines (with emphasis on Neopterin), individual adipose tissue - distribution, and pleiotropic drug effects on the individual course of atherosclerosis and associated cardiovascular disease are reviewed.
Keywords: Adiposity, immune-mediated inflammation, cardiovascular risk, atherosclerotic lesions, metabolic syndrome, adiponectin, monocyte, T-cell, cytokines, Neopterin, cardiovascular disease (CVD), systemic disease, T-lymphocytes, neopterin,obesity, myocardial infarction (MI), homocystein, lowdensity lipoproteins (LDL), atherogenesis, angiogenesis, high sensitive C-reactive protein (hsCRP), intima-media thickness, remodelling, cytokine, chemokine, metalloproteinase, dendritic, foam,osteoclast, nuclear factor, kappaB ligand, osteoprotegerin, T-helper lymphocytes of type 1 (Th-1), reactive oxygen species (ROS), macrophages, monocyte chemotactic protein (MCP), endocannabinoids, oxidation, anti-atherogenic role, sympathetic nervous system, Hypoxia, kappa-B, hypoadiponectinemia, nitric oxide (NO), endothelial NO synthase (eNOS), asymmetric dimethylarginine, bioavailibility, VSMCs, rheumatoid arthritis (RA), systemic lupus erythematodes
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