Question:hard
Which of the following is NOT a predisposing factor for atherosclerotic plaque formation?
Which of the following is NOT a predisposing factor for atherosclerotic plaque formation?
Show Hint
Three relate to lipids, endothelium or oxidation; the protease inhibitor is the odd one out.
Updated On: Jun 24, 2026
- ApoE
- Alpha 2-macroglobulin
- Oxidised LDL
- Increased homocysteine
Show Solution
The Correct Option is B
Solution and Explanation
Approach this by checking each option against the accepted mechanisms of plaque build-up: lipid handling, oxidative modification, endothelial injury and inflammation. Three of the four slot neatly into these pathways, leaving one outlier.
Oxidised LDL is arguably the engine of the lesion. Once LDL infiltrates the intima and is oxidised, macrophages engulf it through scavenger receptors and become lipid-laden foam cells, the very founders of the fatty streak. Raised homocysteine fits too, because it injures endothelium and tips the wall toward thrombosis, a well-documented vascular risk. ApoE belongs as well, since its variants govern how efficiently remnant lipoproteins are cleared, and unfavourable isoforms raise cholesterol and atherosclerotic risk.
Alpha 2-macroglobulin does not fit this scheme. It is a large plasma protease inhibitor that mops up proteinases and binds cytokines as part of general homeostasis; it is not a driver of intimal lipid deposition or plaque growth. By exclusion it is the factor that does not predispose to atherosclerosis.
\[\boxed{\text{Alpha 2-macroglobulin}}\]
Oxidised LDL is arguably the engine of the lesion. Once LDL infiltrates the intima and is oxidised, macrophages engulf it through scavenger receptors and become lipid-laden foam cells, the very founders of the fatty streak. Raised homocysteine fits too, because it injures endothelium and tips the wall toward thrombosis, a well-documented vascular risk. ApoE belongs as well, since its variants govern how efficiently remnant lipoproteins are cleared, and unfavourable isoforms raise cholesterol and atherosclerotic risk.
Alpha 2-macroglobulin does not fit this scheme. It is a large plasma protease inhibitor that mops up proteinases and binds cytokines as part of general homeostasis; it is not a driver of intimal lipid deposition or plaque growth. By exclusion it is the factor that does not predispose to atherosclerosis.
\[\boxed{\text{Alpha 2-macroglobulin}}\]
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