Abstract
LOX-1, a lectin-like 52 kD receptor for oxidized LDL, is present primarily onendothelial cells. It has been linked to endothelial dysfunction, inflammation andoxidative stress. LOX-1 activation has also been linked to collagen formation, akey component of atherosclerotic lesion formation. Recent studies in mousemodels of hyperlipidemia and atherosclerosis demonstrate that deletion of LOX-1sustains endothelial function and inhibits inflammation and oxidative stress,resulting in a marked reduction in the formation of atherosclerotic plaques. Earlystudies demonstrate that LOX-1 abrogation also reduces collagen deposition inatherosclerotic lesions. This review highlights recent findings on the role of LOX-1in the modulation of atherosclerosis and collagen accumulation in theatherosclerotic plaques.
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