Intracellular constituents of ruptured cardiac myocytes can modify LDL via non-oxidative mechanisms, leading to macrophage uptake.
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May link myocyte necrosis to foam cell formation via non-oxidative LDL modification; leaves open relevance to human atherosclerosis.
In this study, the interaction of ruptured cardiac myocytes with low density lipoprotein (LDL) has been investigated and the consequent extent of uptake by macrophages. The results show that lysate released from ruptured myocytes is capable of inducing LDL oxidation and that the resulting modified form is recognised and degraded by macrophages. Peroxyl radical scavengers inhibit the LDL oxidation but not the macrophage uptake suggesting that LDL can be modified by mechanisms that are independent of oxidative processes by intracellular constituents of cardiac myocytes.
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Bourne et al. (1997) studied this question.
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