Key result
The novel lectin-like receptor for ox-LDL (LOX-1) is upregulated by various stimuli and highly expressed in conditions like hypertension and atherosclerosis, contributing to endothelial dysfunction.
The identification of the LOX-1 receptor provides a novel mechanistic target for therapies aimed at treating endothelial dysfunction and atherosclerotic cardiovascular diseases.
Oxidatively modified low-density lipoprotein (ox-LDL) leads to endothelial activation, dysfunction and injury. Recently, a novel lectin-like receptor for ox-LDL (LOX-1) has been identified, primarily in the endothelial cells, and it allows uptake of ox-LDL into endothelial cells. This receptor is transcriptionally upregulated by tumor necrosis factor-alpha, angiotensin II, shear stress and ox-LDL itself. The expression of this receptor activates a variety of intracellular processes that lead to expression of adhesion molecules and endothelial activation. This receptor is highly expressed in the blood vessels of animals and humans with hypertension, diabetes mellitus and atherosclerosis. Expression of this receptor may also be relevant in intra-arterial thrombogenesis and myocardial ischemia-reperfusion injury. Identification and regulation of this receptor and understanding of signal transduction pathways may lead to new therapies of diseases characterized by endothelial dysfunction.
No takes yet. Share an insight, caveat, or question.
Mehta et al. (2002) conducted a review in Endothelial dysfunction, hypertension, diabetes mellitus, and atherosclerosis. LOX-1 (lectin-like oxidized low-density lipoprotein receptor) was evaluated. The novel lectin-like receptor for ox-LDL (LOX-1) is upregulated by various stimuli and highly expressed in conditions like hypertension and atherosclerosis, contributing to endothelial dysfunction.
Synapse has enriched 5 related papers. Consider them for comparative context: