Cellular and cytokine-based inflammatory processes as novel therapeutic targets for the prevention and treatment of atherosclerosis.

摘要: Cardiovascular disease is the largest cause of morbidity and premature mortality its major underlying pathology atherosclerosis. Atherosclerosis commences with deposition lipids in artery wall due to trapping by proteoglycans. Trapped lipoproteins are chemically enzymatically modified yield pro-inflammatory species that induce adhesion molecule expression on endothelial cells leading recruitment multiple immune a chronic inflammatory response. Ongoing remodelling vessel later morphological changes generate "vulnerable" plaques, acute rupture which generates clinical event. The medical therapies anti-hypertensives lipid lowering agents. Although these amongst most efficacious cardiovascular medicine, optimised well-controlled trials maximum effect limited an approximately 30% reduction events. Hence, huge burden remains refractory current atherosclerosis sequelae persist as therapeutic target immense importance. Potential targets include proteoglycan: lipoprotein interaction wall, circulating associated atherogenic system. Anti-inflammatory specific cytokine antagonists neutralizing antibodies, cell depleting antibodies using antigen regulatory T-cells B-cells. In this review, we describe process it involves role inflammation development progression atherosclerotic plaques then manner some processes represent targets.