Ashraf Taye1, Azza A K El-Sheikh. 1. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, Minia, Egypt.
Abstract
BACKGROUND: The role of lectin-like oxidized low-density lipoprotein receptor (LOX)-1 has been implicated in the pathogenesis of different diseases, including atherosclerosis, hypertension, obesity, diabetes mellitus and metabolic syndrome. To date, several studies aimed at partially investigating the mechanistic role of LOX-1 in these various pathologies. Still, so far, the precise signal transduction pathways involving LOX-1 have not yet been elucidated. MATERIALS AND METHODS: The most recent data published by the authors as well as others concerning different pathways involving LOX-1 are collected to formulate the presented updated review. RESULTS: One of the most prominent pathways highlighted in the present review is the relationship of LOX-1 to NADPH oxidase that acts as a major source of harmful free radicals causing oxidative stress in blood vessels. Other pathways involve lipid and glucose metabolism-mediated signal transduction. DISCUSSION: The modulatory role of LOX-1 on nitric oxide and renin/angiotensin systems as well as on fibrosis, apoptosis and inflammatory pathways is discussed. CONCLUSION: The current review revisits LOX-1 and its related pathways, implicating LOX-1 as a target for ameliorating various pathological conditions.
BACKGROUND: The role of lectin-like oxidized low-density lipoprotein receptor (LOX)-1 has been implicated in the pathogenesis of different diseases, including atherosclerosis, hypertension, obesity, diabetes mellitus and metabolic syndrome. To date, several studies aimed at partially investigating the mechanistic role of LOX-1 in these various pathologies. Still, so far, the precise signal transduction pathways involving LOX-1 have not yet been elucidated. MATERIALS AND METHODS: The most recent data published by the authors as well as others concerning different pathways involving LOX-1 are collected to formulate the presented updated review. RESULTS: One of the most prominent pathways highlighted in the present review is the relationship of LOX-1 to NADPH oxidase that acts as a major source of harmful free radicals causing oxidative stress in blood vessels. Other pathways involve lipid and glucose metabolism-mediated signal transduction. DISCUSSION: The modulatory role of LOX-1 on nitric oxide and renin/angiotensin systems as well as on fibrosis, apoptosis and inflammatory pathways is discussed. CONCLUSION: The current review revisits LOX-1 and its related pathways, implicating LOX-1 as a target for ameliorating various pathological conditions.
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