The mechanism of oxidation-induced low-density lipoprotein aggregation: an analogy to colloidal aggregation and beyond?
The mechanism of oxidation-induced low-density lipoprotein aggregation: an analogy to colloidal aggregation and beyond?
复制标题
氧化诱导的低密度脂蛋白聚集的机制:与胶体聚集的类比及其他?
DOI:
10.1016/s0006-3495(01)75887-0
复制
发表时间:
2001
影响因子:
3.4
通讯作者:
Lin,B
中科院分区:
文献类型:
--
作者:
Xu,S;Lin,B
Atherosclerosis is a disease initiated by lipoprotein aggregation and deposition in artery walls. In this study, the de novo low-density lipoprotein aggregation process was examined. Nine major intermediates were identified in two stages of the aggregation process. In the aggregation stage, low-density lipoprotein molecules aggregate and form nucleation units. The nucleation units chain together and form linear aggregates. The linear aggregates branch and interact with one another, forming fractals. In the fusion stage, spatially adjacent nucleation units in the fractal fuse into curved membrane surfaces, which, in turn, fuse into multilamellar or unilamellar vesicles. Alternatively, some adjacent nucleation units in the fractals assemble in a straight line and form rods. Subsequently, the rods flatten out into rough and then into smooth ribbons. Occasionally, tubular membrane vesicles are formed from the fractals. The aggregation stage seems to be analogous to colloidal aggregation and amyloid fiber formation. The fusion stage seems to be characteristic of the lipid-rich lipoproteins and is beyond colloidal aggregation and amyloid fiber formation.