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  Indian J Med Microbiol
 

Figure 1: Pathophysiology of atherogenic dyslipidemia. Generation of small dense-LDL particles (pattern B) and oxidation of LDL particle are key elements in atherosclerosis development. HDL-C antagonizes (-) many of the atherogenic activities of ox-LDL.[2] TG rich LDL is a substrate for hepatic lipase. CE: Cholesteryl esters, CETP: Cholesteryl ester transfer protein, ET cells: Endothelial cells, HDL-C: High-density lipoprotein cholesterol, HL: Hepatic lipase, LOX: Lipoxygenase, LP: Lipoprotein lipase, MPO: Myeloperoxidase, Ox-LDL: Oxidised low-density lipoprotein, SMCs: Smooth muscle cells

Figure 1: Pathophysiology of atherogenic dyslipidemia. Generation of small dense-LDL particles (pattern B) and oxidation of LDL particle are key elements in atherosclerosis development. HDL-C antagonizes (-) many of the atherogenic activities of ox-LDL.[2] TG rich LDL is a substrate for hepatic lipase. CE: Cholesteryl esters, CETP: Cholesteryl ester transfer protein, ET cells: Endothelial cells, HDL-C: High-density lipoprotein cholesterol, HL: Hepatic lipase, LOX: Lipoxygenase, LP: Lipoprotein lipase, MPO: Myeloperoxidase, Ox-LDL: Oxidised low-density lipoprotein, SMCs: Smooth muscle cells