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xidative modification of low density lipoproteins has been a leading hypothesis in atherogenesis, and throughout the 1990's there was intense interest in the discovery of pathways leading to this modification.1,2 In a commentary to an article dealing with 12/15-lipoxygenase gene disruption in the atherosclerotic apolipoprotein E (apoE)-deficient mouse model in 1999, Daniel Steinberg declared "at last direct evidence that lipoxygenases play a role in atherosclerosis."3,4 Since this article seven years ago, the lipoxygenase pathway involvement in atherogenesis has become rather more complicated.
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Colin Funk (2006) studied this question.
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