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由于动脉粥样硬化(AS)而导致的临床事件与沦陷在内膜下基质的LDL氧化直接有关。这些氧化的脂质能激活类似NFkB的转录因子,从而诱导含有NFkB连接位点的一些基因的表达。其蛋白产物能启动炎症反应,首先导致脂质条纹的生成。这一病变的进展与能诱导AS的基因的激活相关联。动脉的钙化改变了动脉壁的力学特性,从而使单核细胞浸润部位的斑块易于破裂。破裂的斑块又使病变部位的组织因子暴露于流动的血液,从而诱发引起临床事件的血栓形成。遗传决定的有效调控系统能阻止脂质氧化,并能使具有重要生物活性的已氧化的脂质失活性,以及调整对氧化脂质的炎症反应。这也许解释了个体和人群对AS形成存在的不同的敏感性。与HDL有关的酶类可能在防止动脉壁脂质氧化中起重要作用。这部分解释了HDL与AS临床事件危险的反相关系。
Clinical events due to atherosclerosis (AS) are directly related to LDL oxidation of the submerged submerged stroma. These oxidized lipids activate transcription factors like NFkB and thus induce the expression of some of the genes that contain the NFkB ligation site. Its protein product initiates an inflammatory response that first leads to the formation of lipid streaks. The progression of this disease is linked to the activation of genes that can induce AS. Arterial calcification alters the mechanical properties of the arterial wall, making the plaque at the mononuclear infiltrate site prone to rupture. In turn, the ruptured plaque exposes the tissue factor in the diseased area to the flowing blood, thereby inducing thrombosis that causes clinical events. The genetically determined and effective regulatory system prevents lipid oxidation, inactivates oxidized lipids of important biological activity, and modulates the inflammatory response to oxidized lipids. This may explain the different sensitivities of individuals and populations to AS formation. HDL-related enzymes may play an important role in preventing lipid oxidation in the arterial wall. This section explains the inverse relationship between the risk of HDL and AS clinical events.