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Within this pathological framework, the oxidation of low-density lipoprotein (LDL) cholesterol represents a critical initiating event, as oxidized LDL (Ox-LDL) triggers a cascade of pro-atherogenic responses: endothelial activation with increased adhesion molecule expression, monocyte recruitment and differentiation into macrophages, and ultimately foam cell formation through unregulated Ox-LDL uptake via scavenger receptors [2]
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Both reactions of this phase are irreversible
Rob Berberian is a double board-certified physician specializing in cosmetic and regenerative medicine
The interplay between mitochondrial dysfunction and ferroptosis during ischemia-associated central nervous system diseases
Liposomal delivery of glutathione: Enhancement of intracellular antioxidant defense
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