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Clin Exp Nephrol. 2004 Sep;8(3):178-82.

Role of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the development of hypertensive organ damage.

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Department of Nephrology and Endocrinology, University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.


Recently, a novel endothelial oxidized low-density lipoprotein (LDL) receptor, lectin-like oxidized LDL receptor (LOX)-1, has been identified by the expression cloning of cultured bovine aortic endothelial cells (BAEC). The experimental evidence has suggested that LOX-1 may contribute to the development of vascular injury. For example, LOX-1 is upregulated in aorta from hypertensive, diabetic, and hyperlipidemic model animals. Also, LOX-1 overexpression is observed in atherosclerotic regions and damaged kidneys. In hypertensive animals, not only antihypertensive drugs but also antioxidant agents suppress the LOX-1 overexpression. Peroxisome proliferator-activated receptor-gamma (PPARgamma) activators inhibit cytokine-stimulated LOX-1 expression, possibly through their antioxidant effects, while, in contrast, LOX-1 generates reactive oxygen species (ROS). Therefore, ROS may play an important role in both the expression and function of LOX-1.

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