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(Circulation Research. 2008;103:1348.)
© 2008 American Heart Association, Inc.

Editorials

Apolipoprotein CIII

A Link Between Hypertriglyceridemia and Vascular Dysfunction?

Sandrine Caron, Bart Staels

From Institut Pasteur de Lille; INSERM; and Université de Lille 2, Faculté des Sciences Pharmaceutiques et Biologiques et Faculté de Médecine, Lille, France.

Correspondence to Bart Staels, Université de Lille 2, Faculté des Sciences Pharmaceutiques et Biologiques et Faculté de Médecine, Lille F-59006, France. E-mail Bart.Staels@pasteur-lille.fr

See related articles, pages 1402–1409

Key Words: apolipoprotein CIII • hypertriglyceridemia • cardiovascular diseases • vascular inflammation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The incidence of obesity-associated disorders, such as type 2 diabetes and the metabolic syndrome, is continuously increasing worldwide.¹ These disorders are characterized by abnormalities in glucose and lipid metabolism, putting patients at increased risk for macro- and microvascular complications.² Although statin treatment, which primarily targets elevated plasma low-density lipoprotein (LDL)-cholesterol levels, lowers cardiovascular morbidity and mortality in patients with type 2 diabetes,³ it is increasingly clear that a significant residual cardiovascular risk remains in these patients,^3–5 which is partly attributable to the typical atherogenic lipoprotein profile (ALP) characterized by hypertriglyceridemia and low high-density lipoprotein (HDL)-cholesterol concentrations.⁶ Post hoc analysis of statin trials, such as PROVE-IT TIMI 22, have identified plasma triglycerides as a determinant of cardiovascular risk in patients achieving LDL-cholesterol goals.⁵

Plasma triglyceride concentrations are determined by the balance between clearance/uptake and production of triglyceride (TG)-rich lipoproteins (7). Dysregulation of this balance results in the development of hypertriglyceridemia.⁷ Triglycerides in very-low-density lipoproteins (VLDL) and chylomicrons are hydrolyzed by lipoprotein lipase, thus allowing their conversion to remnant and subsequently to LDL particles. This process is controlled by specific apolipoprotein (apo) constituents, such as apoCII and apoAV, which facilitate TG-rich lipoprotein clearance/lipolysis, whereas apoCIII delays it.⁸

ApoCIII is a 79-aa glycoprotein synthesized in the liver and the intestine and a major component of the apoB-containing TG-rich lipoproteins and HDL.⁸ Plasma apoCIII levels are positively correlated with plasma triglycerides over the entire spectrum from normo- to hypertriglyceridemia.⁸ ApoCIII deficiency results in hypertriglyceridemia both in humans and mice, whereas overexpression of apoCIII in . . . [Full Text of this Article]

Related Article:

Toll-Like Receptor 2 Mediates Apolipoprotein CIII–Induced Monocyte Activation

Akio Kawakami, Mizuko Osaka, Masanori Aikawa, Satoshi Uematsu, Shizuo Akira, Peter Libby, Kentaro Shimokado, Frank M. Sacks, and Masayuki Yoshida
Circ. Res. 2008 103: 1402-1409. [Abstract] [Full Text] [PDF]