Читать книгу Interventional Cardiology - Группа авторов - Страница 21

LDL particles are well‐known as one of the critical players in the pathogenesis of atherosclerosis, however, the association of LDL amount can cause atherosclerosis remains unclear, even though lowering this lipoprotein reduces atherosclerosis‐related cardiovascular events [7, 29–31]. On the other hand, even though both LDL and high‐density lipoprotein (HDL) particles are highly heterogenous [32], plasma HDL‐cholesterol concentrations are negatively associated with atherosclerosis [29,33]. Interestingly, raising plasma HDL‐cholesterol concentrations did not show any benefit on existing atherosclerosis [34], which might suggest that HDL function may play a more pivotal part in the prevention against atherosclerosis by averting endothelial activation and enhance NO production []. LDL can deposit in the arterial wall due to impaired endothelial barrier function and retain within the intimal layer by extracellular matrix macromolecules [38]. Enormous researches demonstrated that the oxidisation of LDL particles including ROS formation in the intimal wall due to metal ion catalysis could initiate atherogenesis [39,40]. Oxidised LDL is the major modified form of native LDL since structurally it is very prone to oxidative damage [41]. The oxidised LDL particles serves as ligands for the scavenger receptors (SRs) that facilitate macrophage foam cell formation which is the hallmark of early atherosclerotic lesions that subsequently promoting humoral and adaptive immunity leading to plaque formation [7,42,43].