Price Matthew J, Shah Prediman K
Division of Cardiology and Atherosclerosis Research Center, Burns and Allen Research Institute, Los Angeles, CA, USA.
Rev Cardiovasc Med. 2002 Summer;3(3):129-37.
The development of atherosclerosis is a complex process whose central elements include the entrapment of low-density lipoprotein in the vessel wall, its subsequent oxidative modification, and the stimulation of proinflammatory gene expression leading to inflammatory cell recruitment, infiltration, and activation. High-density lipoprotein interacts with this process at multiple points, and these interactions could provide therapeutic targets to prevent, stabilize, or even promote the regression of atherosclerosis. High-density lipoprotein may retard atherosclerotic progression by promoting cholesterol efflux from the arterial wall, thereby reducing plaque lipid content as well as potentially inhibiting nascent fatty streak formation. A growing body of evidence derived from clinical trials supports the contention that the raising of high-density lipoprotein levels may confer significant cardiovascular benefit independently of low-density lipoprotein lowering. An antiatherogenic strategy focusing on high-density lipoprotein and its apolipoproteins represents a new frontier in the management of atherosclerosis.
