Current concepts in cardiovascular pathology: The role of LDL cholesterol in plaque rupture and stabilization
Current concepts in cardiovascular pathology: The role of LDL cholesterol in plaque rupture and stabilization
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DOI：
10.1016/s0002-9343(98)00041-2
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发表时间：
1998-02-23
影响因子：
5.9
通讯作者：
Ganz, Peter
中科院分区：
文献类型：
--
作者：
Libby, Peter;Schoenbeck, Uwe;Ganz, Peter
新出现的证据正在重新定义冠状动脉粥样硬化的传统概念。最近的数据表明，严重的狭窄，传统的关注焦点，不会导致大多数冠状动脉事件。相反，人们对狭窄程度较低但更脆弱的病变的兴趣有所增加，这些病变的特征是薄纤维帽、大量脂质积聚、大量巨噬细胞和平滑肌细胞耗竭。这种病变似乎容易破裂，这使得血液与斑块脂质核心中的高度血栓形成物质接触，从而促进血栓形成。纤维帽可能会因细胞外基质合成减少或基质降解增加而变得脆弱。由T淋巴细胞产生的细胞因子干扰素-γ抑制平滑肌细胞合成胶原蛋白的能力，胶原蛋白是纤维帽的结构重要组分。一个被称为基质金属蛋白酶的酶家族可以降解血管细胞外基质的所有主要成分：胶原蛋白、弹性蛋白和蛋白聚糖。对动脉粥样硬化生化机制的进一步研究可能会更全面地了解降脂治疗的临床益处。
Emerging evidence is redefining traditional concepts of coronary atherosclerosis. Recent data indicate that severe stenoses, the traditional focus of attention, do not cause most coronary events. Rather, interest has increased in the often less stenotic but more vulnerable lesions that are characterized by thin fibrous caps, large lipid accumulations, large numbers of macrophages, and depletion of smooth muscle cells. Such lesions appear prone to rupture, which allows the blood to come into contact with the highly thrombogenic material in the lipid core of the plaque, thereby precipitating thrombosis. The fibrous cap may become weakened through decreased synthesis of the extracellular matrix or increased degradation of the matrix. The cytokine interferon-gamma, produced by T-lymphocytes, inhibits the ability of smooth muscle cells to synthesize collagen, a structurally important component of the fibrous cap. A family of enzymes known as matrix metalloproteinases can degrade all major constituents of the vascular extracellular matrix: collagen, elastin, and proteoglycans. Additional studies on the biochemical mechanisms of atherosclerosis may provide a fuller understanding of the ways in which lipid-lowering therapy can confer clinical benefit.