Oxidized Low-density Lipoprotein and Atherosclerosis

Abstract Atherosclerosis is a chronic inflammatory disease characterized by lipid buildup and immune response dysregulation in the artery walls. One of the important participants is oxidized low-density lipoprotein (OxLDL), which is involved in both the initiation and progression of atherosclerosis. OxLDL is generated through the oxidative alteration of native low-density lipoprotein particles, primarily in the subendothelial region, which is triggered by reactive oxygen species and oxidizing enzymes. These alterations have proinflammatory, immunogenic, and cytotoxic effects that impair endothelial homeostasis, increase adhesion molecules, and encourage monocyte recruitment. Within the intima, macrophages ingest OxLDL through scavenger receptors such as CD36, SR-A, and Lox-1, resulting in foam cell production and the expansion of the lipid-rich necrotic core. Aside from macrophages, OxLDL modulates smooth muscle cell migration, apoptosis, and phenotype modification, all of which contribute to plaque complications and instability. It also functions as a neoantigen, activating adaptive immune responses and causing chronic vascular inflammation. Increased blood OxLDL levels are associated with an increased risk of cardiovascular disease and plaque burden. While traditional lipid-lowering medications indirectly improve OxLDL effects, emerging techniques such as scavenger receptor inhibitors, immunotherapies, and target antioxidants have the potential for more precise involvement. This study covers the molecular processes through which OxLDL participates in atherogenesis and explores emerging treatment options for controlling its harmful effect.