(Auto)Phagocytosis in Atherosclerosis: Implications for Plaque Stability and Therapeutic Challenges

摘要: This chapter is intended to describe the interactions between cell death, phagocytosis and autophagic survival in atherosclerosis, how these processes could be attractive therapeutic targets for atherosclerotic plaque stabilization. Atherosclerosis a long-term, progressive inflammatory disease characterized by formation of plaques intima mediumand large-sized arteries. Progression accelerated well-known risk factors including gender, age, hypercholesterolemia, diabetes mellitus, hypertension, smoking, obesity sedentary life-style (Kannel et al., 2004). In advanced stage, can partially or totally occlude blood vessel, known as arterial stenosis. However, not only degree stenosis, but also composition stability determines clinical outcome (Hansson, 2005). Indeed, may become extremely unstable prone rupture through presence many cells mediators, large necrotic core consisting uncleared debris lipids, high death leading scarce amount smooth muscle cells, leaky neovessels inside plaque. Occlusive thrombi, result rupture, turn cause acute (and often fatal) manifestations, such myocardial infarction stroke. Current therapy focused on chirurgical interventions (stents, endarterectomy, bypass) plasma cholesterol lowering drugs (e.g. statins). addition, changes diet exercise have made significant inroads preventing atherothrombotic events (Getz & Reardon, 2006). Although aforementioned approaches provided improvements, they are far from sufficient. Analysis machinery well strategies provide additional insights development new stabilizing strategies.