Abstract
Atherosclerosis is a multifactorial disease whose pathogenesis is still unclear. Mounting evidence, however, supports the concept that subendothelial retention of apoB100-containing lipoproteins is the initiating event in atherogenesis. Subsequently, a series of biological responses to this retained material leads to specific molecular and cellular processes that promote lesion formation.
Keywords: Apolipoprotein B, atherosclerosis, proteoglycan, retention, glycos aminoglycan, transgenic mice
Footnotes
Received 3 July 2003; received after revision 13 August 2003; accepted 15 August 2003