Which sequence describes how LDL contributes to foam cell formation in the arterial wall?

Which sequence describes how LDL contributes to foam cell formation in the arterial wall?

• A. LDL is filtered into the lumen; HDL removes cholesterol; smooth muscle migrates.
• B. LDL binds to HDL to form foam cells.
• C. LDL enters sub-endothelial space and is taken up by macrophages to form foam cells.
• D. Smooth muscle cells migrate to the intima to form foam cells.

Answer: (C)

Foam cells form when macrophages in the arterial wall ingest lipids that have leaked into the sub-endothelial space from LDL particles. LDL migrates into the intima and becomes modified (often oxidized); macrophages take up this modified LDL via scavenger receptors. This uptake is not downregulated as lipid content rises, so cholesterol accumulates inside the macrophages and they become lipid-laden foam cells, driving the fatty streak in early atherosclerosis. HDL’s normal role is to remove cholesterol from tissues and transport it to the liver, not to form foam cells. While smooth muscle cells can migrate to the intima and contribute to plaque structure, the classic foam cell formation is driven by macrophage uptake of LDL in the sub-endothelial space.

Foam cells form when macrophages in the arterial wall ingest lipids that have leaked into the sub-endothelial space from LDL particles. LDL migrates into the intima and becomes modified (often oxidized); macrophages take up this modified LDL via scavenger receptors. This uptake is not downregulated as lipid content rises, so cholesterol accumulates inside the macrophages and they become lipid-laden foam cells, driving the fatty streak in early atherosclerosis. HDL’s normal role is to remove cholesterol from tissues and transport it to the liver, not to form foam cells. While smooth muscle cells can migrate to the intima and contribute to plaque structure, the classic foam cell formation is driven by macrophage uptake of LDL in the sub-endothelial space.