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Curr Med Chem. 2018 May 7. doi: 10.2174/0929867325666180508100950. [Epub ahead of print]

Role of Ox-LDL and LOX-1 in Atherogenesis.

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1
Division of Cardiology, Central Arkansas Veterans Healthcare System and the University of Arkansas for Medical Sciences, Arkansas. United States.

Abstract

Oxidized LDL (ox-LDL) plays a central role in atherosclerosis by acting on multiple cells such as endothelial cells, macrophages, platelets, fibroblasts and smooth muscle cells through LOX-1. LOX-1 is a 50 kDa transmembrane glycoprotein that serves as receptor for ox-LDL, modified lipoproteins, activated platelets and advance glycation end-products. Ox-LDL through LOX-1, in endothelial cells, cause increase in leukocyte adhesion molecules, activates pathways of apoptosis, increase reactive oxygen species and cause endothelial dysfunction. In vascular smooth muscle cells and fibroblasts, they stimulate proliferation, migration and collagen synthesis. LOX-1 expressed on macrophages inhibit macrophage migration and stimulate foam cell formation. They also stimulates generation of metalloproteinases and contributes to plaque instability and thrombosis. Drugs that modulates LOX-1 are desirable targets against atherosclerosis. Many naturally occurring compounds have been shown to modulate LOX-1 expression and atherosclerosis. Currently novel drug design techniques are used to identify molecules that can bind to LOX-1 and inhibit its activation by ox-LDL. In addition, techniques using RNA interference and monoclonal antibody against LOX-1 are currently being investigated for clinical use.

KEYWORDS:

Endothelial cells LOX-1; LOX-1 atherosclerosis; Ox-LDL and LOX-1; Oxidized LDL.; oxidative stress LOX-1

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