Jang I K, Lassila R, Fuster V
Cardiac Unit, Massachusetts General Hospital, Boston 02114.
Eur Heart J. 1993 Dec;14 Suppl K:2-6.
Following endothelial injury, monocytes attach to the subendothelium and penetrate into the vessel wall, forming macrophage/foam cells by accumulating lipids. Macrophages release various products such as interleukins, complement factor fragments, tumour necrosis factors, oxidized cholesterol, and oxygen free radicals, leading to further endothelial injury and cytolysis. Platelets at the site of vascular injury, monocytes, endothelial cells, and smooth muscle cells release mitogenic factors which stimulate smooth muscle cell proliferation and migration. This smooth muscle cell proliferation, together with organization of thrombus and extracellular matrix synthesis, leads to the development of atheromatous plaques. Macrophages, by releasing proteases such as collagenase and elastase, form an abscess in the plaque which is covered by a thin fibrous cap. When this cap ruptures, a local thrombus is formed and depending upon the degree and duration of thrombus, and the degree of collateral development the fate of this thrombotic process is determined.
内皮损伤后，单核细胞黏附于内皮下并穿透进入血管壁，通过蓄积脂质形成巨噬细胞/泡沫细胞。巨噬细胞释放多种产物，如白细胞介素、补体因子片段、肿瘤坏死因子、氧化胆固醇和氧自由基，导致进一步的内皮损伤和细胞溶解。血管损伤部位的血小板、单核细胞、内皮细胞和平滑肌细胞释放促有丝分裂因子，刺激平滑肌细胞增殖和迁移。这种平滑肌细胞增殖，连同血栓形成和细胞外基质合成，导致动脉粥样硬化斑块的形成。巨噬细胞通过释放诸如胶原酶和弹性蛋白酶等蛋白酶，在斑块内形成脓肿，脓肿被一层薄的纤维帽覆盖。当这层纤维帽破裂时，就会形成局部血栓，根据血栓的程度和持续时间以及侧支循环发育程度来决定这个血栓形成过程的结局。
