Oksjoki Riina, Kovanen Petri T, Pentikäinen Markku O
Wihuri Research Institute, Helsinki, Finland.
Curr Opin Lipidol. 2003 Oct;14(5):477-82. doi: 10.1097/00041433-200310000-00008.
Atherosclerosis is characterized by a strong inflammatory component. One factor contributing to inflammation in the arterial intima is the complement system. Here we summarize recent progress in the field of complement research on atherogenesis.
The complement system is activated in human atherosclerotic lesions and is actively regulated by the local synthesis of complement components and of complement regulatory proteins. Potential triggers of complement activation in the arterial intima include immunocomplexes, C-reactive protein, modified lipoproteins, apoptotic cells, and cholesterol crystals. Complement activation releases anaphylatoxins, and anaphylatoxin receptors have been identified in human atherosclerotic lesions. However, experiments on genetically engineered mice with severe hyperlipidemia have been unable to show a major role for complement in experimental atherogenesis.
In humans there is extensive circumstantial evidence for a role of complement in atherosclerosis, which is somewhat contradictory to recent modest or negative findings in atherosclerosis-prone genetically engineered hyperlipidemic mice.
动脉粥样硬化的特征是具有强烈的炎症成分。补体系统是导致动脉内膜炎症的一个因素。在此，我们总结补体研究领域中动脉粥样硬化发生机制的最新进展。
补体系统在人类动脉粥样硬化病变中被激活，并通过补体成分和补体调节蛋白的局部合成受到积极调控。动脉内膜中补体激活的潜在触发因素包括免疫复合物、C反应蛋白、修饰的脂蛋白、凋亡细胞和胆固醇晶体。补体激活释放过敏毒素，并且在人类动脉粥样硬化病变中已鉴定出过敏毒素受体。然而，对患有严重高脂血症的基因工程小鼠进行的实验未能显示补体在实验性动脉粥样硬化发生中起主要作用。
在人类中，有大量间接证据表明补体在动脉粥样硬化中起作用，这与最近在易患动脉粥样硬化的基因工程高脂血症小鼠中得到的适度或阴性结果有些矛盾。
