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By modulating RAB40C-dependent lipid droplet homeostasis and suppressing mitochondrial ROS generation, this approach can simultaneously inhibit foam cell formation and oxidative stress damage, thereby offering a promising early intervention strategy to arrest the progression of atherosclerosis

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aureus and staphylococcal complement inhibitor A interfere with complement activation by inactivating complement components and blocking immune cell chemotaxis, thus reducing immune cell recruitment to the infection site [28]