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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:2211.)
© 2004 American Heart Association, Inc.

Brief Reviews

Molecular Interactions Leading to Lipoprotein Retention and the Initiation of Atherosclerosis

Maged F. Khalil; William D. Wagner; Ira J. Goldberg

From the Division of Preventive Medicine & Nutrition (M.F.K., I.J.G.), Columbia University College of Physicians & Surgeons, New York, NY; and the Department of Pathology (W.D.W.), Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to Ira J. Goldberg, MD, Division of Preventive Medicine & Nutrition, Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032. E-mail ijg3{at}columbia.edu

Atherosclerosis is distinguished by the accumulation of lipoprotein lipid within the arterial wall. An ionic interaction of positively charged regions of apolipoprotein (apo) B with matrix proteins, including proteoglycans, collagen, and fibronectin, is thought to initiate this process. Proteoglycans are complex glycoproteins containing highly negatively charged carbohydrate chains. These proteins are abundant in atherosclerosis lesions, and they associate with apoB-containing lipoproteins. Several specific regions of apoB may mediate this process. Other lipoprotein-associated proteins, including apoE and lipases, might also participate in this process. In addition, retention may occur via lipoprotein association with other matrix molecules or as a consequence of intra-arterial lipoprotein aggregation.

Atherosclerosis is initiated by the accumulation of lipoprotein lipid within the artery wall. This process is thought to involve an ionic interaction between apoB and proteoglycans. Lipoprotein aggregation and association with other matrix proteins are likely additional routes to lipoprotein retention.

Key Words: atherosclerosis • lipoproteins • apolipoproteins • proteoglycans

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