Kruth H S
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1422, USA.
Curr Mol Med. 2001 Dec;1(6):633-53. doi: 10.2174/1566524013363212.
Progressive accumulation of cholesterol in the arterial wall causes atherosclerosis, the pathologic process underlying most heart attacks and strokes. Low density lipoprotein (LDL), the major carrier of blood cholesterol, has been implicated in the buildup of cholesterol in atherosclerotic plaques. Endothelial cells that line arteries function to transport LDL into the vessel wall. Models for the mechanism of cholesterol accumulation in atherosclerotic plaques emphasize increased LDL uptake into the vessel wall or increased retention of LDL that has entered the vessel wall. This article reviews the pathways of cholesterol entry and removal, the metabolism, and the physical changes of cholesterol in the vessel wall. How these processes are believed to contribute to cholesterol buildup in atherosclerotic plaques is discussed.
动脉壁中胆固醇的逐渐积累会导致动脉粥样硬化,这是大多数心脏病发作和中风的病理过程。低密度脂蛋白(LDL)是血液中胆固醇的主要载体,与动脉粥样硬化斑块中胆固醇的积累有关。动脉内壁的内皮细胞负责将LDL转运到血管壁中。动脉粥样硬化斑块中胆固醇积累机制的模型强调血管壁对LDL摄取增加或进入血管壁的LDL潴留增加。本文综述了胆固醇进入和清除的途径、代谢以及血管壁中胆固醇的物理变化。文中还讨论了这些过程被认为是如何导致动脉粥样硬化斑块中胆固醇积累的。