Xun Wang1, Daniel J Rader. 1. Institute for Translational Medicine and Therapeutics and Cardiovascular Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6160, USA.
Abstract
PURPOSE OF REVIEW: Macrophage reverse cholesterol transport is one of the key mechanisms mediating the protective effects of high-density lipoproteins on atherosclerosis. This review focuses on the recent developments in our understanding of molecular mechanisms of macrophage reverse transport and regulators that play important roles during this process. RECENT FINDINGS: Macrophage reverse cholesterol transport is promoted by apolipoprotein A-I overexpression and reduced in the setting of apolipoprotein A-I deficiency. A liver X receptor agonist markedly increases macrophage reverse cholesterol transport. ATP-binding cassette transporter A1 and ATP-binding cassette transporter G1 are liver X receptor-responsive macrophage genes that promote cholesterol efflux to lipid-free apolipoprotein A-I and mature high-density lipoprotein, respectively. The direct roles of ATP-binding cassette transporter A1 and ATP-binding cassette transporter G1 in macrophage reverse cholesterol transport in vivo remain unclear. Therapeutically promoting macrophage reverse cholesterol transport has been recognized as one of the promising means to prevent atherosclerosis. SUMMARY: Increasing evidence has suggested that ATP-binding cassette transporter A1 and ATP-binding cassette transporter G1 are involved in macrophage reverse cholesterol transport. In-depth understanding of the molecular mechanisms will enable us to develop new therapeutic means to protect against atherosclerosis.
PURPOSE OF REVIEW: Macrophage reverse cholesterol transport is one of the key mechanisms mediating the protective effects of high-density lipoproteins on atherosclerosis. This review focuses on the recent developments in our understanding of molecular mechanisms of macrophage reverse transport and regulators that play important roles during this process. RECENT FINDINGS: Macrophage reverse cholesterol transport is promoted by apolipoprotein A-I overexpression and reduced in the setting of apolipoprotein A-I deficiency. A liver X receptor agonist markedly increases macrophage reverse cholesterol transport. ATP-binding cassette transporter A1 and ATP-binding cassette transporter G1 are liver X receptor-responsive macrophage genes that promote cholesterol efflux to lipid-free apolipoprotein A-I and mature high-density lipoprotein, respectively. The direct roles of ATP-binding cassette transporter A1 and ATP-binding cassette transporter G1 in macrophage reverse cholesterol transport in vivo remain unclear. Therapeutically promoting macrophage reverse cholesterol transport has been recognized as one of the promising means to prevent atherosclerosis. SUMMARY: Increasing evidence has suggested that ATP-binding cassette transporter A1 and ATP-binding cassette transporter G1 are involved in macrophage reverse cholesterol transport. In-depth understanding of the molecular mechanisms will enable us to develop new therapeutic means to protect against atherosclerosis.
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