Possible biological mechanisms that make low density lipoproteins a risk factor in atherogenesis.
Low density lipoprotein (LDL) is a risk factor in the development of atherosclerosis. The biological mechanism for this association has been obscure. This paper shows that LDL can be modified in vitro by several chemical and biological means. Modified forms of LDL seem to make it susceptible to enhanced uptake in macrophages. LDL may also induce disturbance of the surrounding cells, especially endothelial cells, as it is potentially cytotoxic. An hypothesis is presented based on the fact that LDL is a labile lipoprotein and may, while situated in the arterial wall, undergo modifications and thereby lead to lipid deposition.
D001161:Arteriosclerosis / Q000503:physiopathology*; D002478:Cells, Cultured; D004727:Endothelium / Q000378:metabolism; D005487:Foam Cells / Q000502:physiology; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008077:Lipoproteins, LDL / Q000097:blood*; D008264:Macrophages / Q000502:physiology; D012306:Risk; D014471:Umbilical Veins / Q000378:metabolism
D008077:Lipoproteins, LDL; D006861:Hydrogen Peroxide