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Atherosclerotic plaque formation refers to the pathophysiological process whereby fatty deposits (plagues) composed of lipids, cholesterol, calcium, inflammatory cells, and cellular debris accumulate within the intimal layer of arteries, leading to vessel wall thickening and loss of elasticity[1][7]. This process triggers a chronic inflammatory response involving endothelial injury, monocyte/macrophage infiltration, foam cell and extracellular matrix deposition, and, over time, the formation of stable or unstable plaques. Plaque rupture or erosion can result in thrombosis and downstream vascular occlusion, manifesting clinically as heart attack, stroke, or other forms of ischemic disease[1][4][10]. While individual molecular targets in this pathway (e.g., LDL, inflammatory cytokines, specific immune cell subsets, NLRP3 inflammasome) are the focus of therapeutic interventions, "atherosclerotic plaque formation" itself is not a discrete molecular target, but rather a complex, multifactorial disease process.
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