Gianturco S H, Bradley W A
Department of Medicine, Baylor College of Medicine, Houston, TX 77030.
Semin Thromb Hemost. 1988 Apr;14(2):165-9. doi: 10.1055/s-2007-1002770.
Structurally and functionally abnormal VLDL exist in hypertriglyceridemic humans. These large abnormal VLDL, in contrast to large normal VLDL, interact with cell surface receptors. One large VLDL particle carries far more total cholesterol than one LDL particle. Receptor-mediated uptake of abnormal VLDL is injurious to endothelial cells and converts macrophages into foam cells in vitro. These observations lead to the hypothesis that if similar phenomena occur in vivo, abnormal VLDL, which have prolonged residence times and increased opportunity to interact with arterial cells, are atherogenic by promoting endothelial injury and initiating foam cell formation. Since premature atherosclerosis is associated with some forms of hypertriglyceridemia and foam cells accumulate in certain hypertriglyceridemic subjects, similar events may indeed occur in vivo.
结构和功能异常的极低密度脂蛋白（VLDL）存在于高甘油三酯血症患者中。与正常的大颗粒VLDL相比，这些异常的大颗粒VLDL会与细胞表面受体相互作用。一个大颗粒VLDL携带的总胆固醇比一个低密度脂蛋白（LDL）颗粒多得多。受体介导的异常VLDL摄取对内皮细胞具有损害作用，并在体外将巨噬细胞转化为泡沫细胞。这些观察结果引出了一个假设：如果体内发生类似现象，那么具有较长停留时间且与动脉细胞相互作用机会增加的异常VLDL，会通过促进内皮损伤和引发泡沫细胞形成而具有致动脉粥样硬化作用。由于早发性动脉粥样硬化与某些形式的高甘油三酯血症相关，并且在某些高甘油三酯血症患者中会积累泡沫细胞，类似事件在体内可能确实会发生。
