Fig. 2. Foam cell formation and metabolism of OxLDL in atherosclerotic lesions. LDL particles are transferred into the vessel wall tissues, where they are oxidized. After the oxidation of LDL, the resulting OxLDL is recongnized by scavenger receptors and taken up by macrophages. A portion of the intimal smooth muscle cells dedifferentiate and migrate into the area of intimal thickening. Activated smooth muscle ce lls are also able to accumulate OxLDL. OxLDL is degraded in lysosomes after being taken up by the cells, but this degradation is not fully completed. Partially degraded modified apoB fragments thus accumulate in the lesions. Fig. 3. Systemic behavior of OxLDL. OxLDL is thought to be generated in vessel wall tissues even in the early phase of atherogenesis. OxLDL gradally accumulates in premature lesions, while OxLDL migrates between the vessel wall and the circulation. When plaque is damaged, a thrombus is generated and the blood flow is occluded. In the acute phase upon plaque ruptures, a portion of the intact OxLDL and degraded OxLDL which has accumulated in the lesions is released into the circulation. In the peripheral blood, the OxLDL level go up in the acute phase, and it then goes down as OxLDL is cleared by the liver from the circulation. levels using the mAb EO6. They have also reported increased OxLDL levels in patients with AMI. The OxLDL levels increased in the acute phase or after percutaneous intervention and trans- plantation,(21,22) suggesting that plaque injury after spontaneous rupture or clinical treatment would release OxLDL from the atherosclerotic lesions into the circulation. These observations taken together support the concept that OxLDL is released from ruptured lesions into the circulation. A commercial kit to measure OxLDL is available from the Mercodia AB (Uppsala, Sweden). A number of studies were carried out using it, and an increase in the plasma OxLDL concen- tration in the patients with plaque instability was demonstrated.(23) H. Itabe J. Clin. Biochem. Nutr. | July 2012 | vol. 51 | no. 1 | 3 ©2012 JCBN