Kadish J L
Atherosclerosis. 1979 Aug;33(4):409-13. doi: 10.1016/0021-9150(79)90033-9.
It has recently been found that endothelial cells exhibit an unusual change in cellular behavior in response to contact with fibrin. The possible implications of this finding with regard to the mechanism of atherogenesis are discussed. It is proposed that mural fibrin in vivo may produce a disorganized endothelium which can act as a nidus for further fibrin deposition and platelet aggregation. In the presence of inadequate fibrinolysis, a prolonged endothelial lesion could occur which may eventually result in atheromatous plaque formation. This view of atherogenesis requires reduced fibrinolytic activity as a prerequisite for plaque formation, a requirement which is in agreement with currently known data associating atherogenic risk factors with inhibited fibrinolysis.
最近发现，内皮细胞在与纤维蛋白接触时会表现出异常的细胞行为变化。讨论了这一发现对动脉粥样硬化发生机制的可能影响。有人提出，体内的壁内纤维蛋白可能会使内皮紊乱，而这种紊乱的内皮可作为进一步纤维蛋白沉积和血小板聚集的病灶。在纤维蛋白溶解不足的情况下，可能会出现长时间的内皮损伤，最终可能导致动脉粥样斑块形成。这种动脉粥样硬化发生的观点要求纤维蛋白溶解活性降低作为斑块形成的先决条件，这一要求与目前已知的将动脉粥样硬化危险因素与纤维蛋白溶解抑制相关联的数据一致。
