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The progression from a completely normal artery to a clogged or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues fixing the apoB containing particles in place AND making more space for more of them

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However, many questions remain unclear about this process, such as how LDs trigger endocytosis at the cell surface, the relevant recognition receptors, and whether LDs entering the cell are rapidly broken down by lysosomes