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CYP2E1 and CYP4A as microsomal catalysts of lipid peroxides in murine nonalcoholic steatohepatitis

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Summary Atherosclerotic lesions initiate with endothelial cell dysfunction causing modification of apoB containing lipoproteins (LDL, VLDL, remnants) and infiltration of immune cells, particularly monocytes, into the subendothelial space (Figure 1)