If immune cells in atherosclerotic plaques excessively produce TNF-α, which consequence is most likely regarding plaque stability?

💡 Explanation

TNF-α stimulates matrix metalloproteinase (MMP) production by macrophages within atherosclerotic plaques, because TNF-α activates NF-κB, which upregulates MMP gene expression. Therefore, MMPs degrade the collagen-rich extracellular matrix, weakening the plaque and increasing the risk of rupture, rather than stabilizing it with collagen or reducing foam cell formation.

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