Atherosclerosis and molecular pathology: Mechanisms of cholesteryl ester accumulation in foam cells and extracellular space of atherosclerotic lesions.

In vivo action of 15-lipoxygenase in early stages of human atherogenesis.

“…Long-lasting hypercholesterolemia is of major importance, but beyond cholesterol there may be other factors of patho-physiological relevance (3). A key event in early atherogenesis is the formation of lipid loaded foam cells that accumulate in the subendothelial space of the arteries to form the fatty streaks generally accepted as early atherosclerotic lesions (4). Although the mechanism of foam cell formation in vivo is unclear it has been suggested that foam cells develop from peripheral monocytes/macrophages or from smooth muscle cells by taking up modified LDL via scavenger receptor mediated pathways (5,6).…”

Lipoxygenase treatment render low-density lipoprotein susceptible to Cu2+-catalysed oxidation

“…Oxidative modification of low-density lipoprotein (LDL) is implicated as an early event in atherogenesis [1][2][3]. Oxidatively modified LDL is rapidly taken up by macrophages and smoothmuscle cells [4] via scavenger-receptor-mediated pathways [5]. In contrast with the LDL-receptor pathway, the scavenger-receptor pathways are not feed-back controlled.…”

The Rabbit 15-Lipoxygenase Preferentially Oxygenates LDL Cholesterol Esters, and This Reaction Does Not Require Vitamin E

“…Foam cells develop from peripheral monocytes or from smooth muscle cells by taking up modified low density lipoprotein (LDL) 1 via scavenger receptor(s) or oxidized LDL receptor(s)-mediated pathways (3,4). In vivo LDL oxidation is thought to be a major LDL-modifying process, and the lipidperoxidizing enzyme 15-lipoxygenase (15-LOX) may be involved.…”