In atherosclerosis, the following process happens:
- Lipid deposits of LDL-cholesterol happen on the endothelium
- They triggers an inflammatory reaction of the endothelium: macrophages circulating in the bloodstream comes in and assimilates the LDL-cholesterol
- The macrophage enters apoptosis when they are full of LDL-cholesterol, and this triggers collagen production which ends in creating a plaque
My question is: in a common inflammatory reaction, the secretion of caspase triggers the apoptosis of the macrophages that have assimilated foreign material. Then the macrophages migrate to lysosomes where they are degraded. Why does this migration not happen in atherosclerosis?
Might be linked with this question: Why oxLDL accumulate to form foam cells?