Navab M, Fogelman A M, Berliner J A, Territo M C, Demer L L, Frank J S, Watson A D, Edwards P A, Lusis A J
Department of Medicine, University of California, Los Angeles, USA.
Am J Cardiol. 1995 Sep 28;76(9):18C-23C. doi: 10.1016/s0002-9149(99)80466-4.
The earliest lesion in the development of an atherosclerotic plaque is the fatty streak. This chronic inflammatory reaction results from a sequence of events that begins with the trapping of low density lipoprotein (LDL) in the subendothelial space of the artery wall. The trapped LDL is seeded with oxidative species released by the overlying endothelium, and lipid oxidation is initiated within the LDL particle. Some of the lipids that result lead to the activation of NFkB-like transcription factors that cause the expression of genes whose protein products mediate monocyte binding, monocyte chemotaxis into the subendothelial space, and conversion into macrophages. At least 1 major gene modulates the oxidation of LDL lipids and/or the biologic response to these lipids. The inverse relation between high density lipoprotein (HDL) and atherosclerotic events may in part be due to enzymes associated with HDL that destroy the biologically active lipids generated in LDL.
动脉粥样硬化斑块发展过程中最早出现的病变是脂纹。这种慢性炎症反应源于一系列事件，这些事件始于低密度脂蛋白（LDL）在动脉壁内皮下间隙的蓄积。蓄积的LDL与覆盖其上的内皮细胞释放的氧化物质结合，LDL颗粒内开始脂质氧化。由此产生的一些脂质会激活类NFkB转录因子，这些因子会导致某些基因的表达，其蛋白质产物介导单核细胞结合、单核细胞趋化进入内皮下间隙并转化为巨噬细胞。至少有1个主要基因调节LDL脂质的氧化和/或对这些脂质的生物学反应。高密度脂蛋白（HDL）与动脉粥样硬化事件之间的负相关关系可能部分归因于与HDL相关的酶，这些酶会破坏LDL中产生的生物活性脂质。
