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?

  • $\begingroup$ Why do you write "the macrophages migrate to lysosomes"? $\endgroup$
    – Bryan Krause
    Jul 17 at 1:35
  • $\begingroup$ I think you have some problems with your terms - perhaps look up what lysosomes are, and whether this might be something that a macrophage could migrate to? You might also want to look up whether caspases are secreted for initiation of apoptosis. $\endgroup$
    – bob1
    Jul 17 at 2:43
  • $\begingroup$ @bob1 Thanks but could you please be more specific about the interrogation? For caspase for example, I have read an article about a study asking whether caspase triggering apoptosis is a unique or multiple effect of caspase. What is the problem with that? $\endgroup$ Jul 17 at 21:05
  • $\begingroup$ The term "secrete" means a specific something in biology and I don't think you are using it correctly. Caspases do trigger apoptosis, but is this done by secretion of the caspases or not? $\endgroup$
    – bob1
    Jul 17 at 21:56
  • $\begingroup$ My understanding is that caspase is secreted by cells and that caspase triggers apoptosis by linking to chemical receptors on other cells $\endgroup$ Jul 19 at 10:23


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