LOX-1, or lectin-like oxidized low-density lipoprotein receptor 1, is a transmembrane glycoprotein that binds and internalizes oxidized low-density lipoprotein (ox-LDL) in foam cells. It is the main receptor for ox-LDL and belongs to the scavenger receptor family, which is associated with various cardiovascular diseases, particularly atherosclerosis. LOX-1 plays a critical role in the formation of atherosclerotic plaques in the endothelial intimal layer, which can evolve into complicated thrombi involving fibroblasts, activated platelets, apoptotic muscle cells, and macrophages transformed into foam cells. This process disrupts vascular endothelial homeostasis, leading to partial or total obstruction of blood vessels and potentially causing myocardial ischemia. LOX-1 is also involved in other pathologies such as obesity and diabetes mellitus. LOX-1 is a 50 kDa transmembrane glycoprotein that undergoes post-translational modifications, including N-glycosylation, which is essential for its function. It is expressed in macrophages, vascular smooth muscle cells, cardiomyocytes, platelets, and fibroblasts. LOX-1 has a secondary role in endothelial dysfunction and apoptosis. Mutations and polymorphisms in the LOX-1 gene can influence its function, with some variants, like LOXIN, potentially offering protective effects by blocking LOX-1 activation. LOX-1 is also involved in the development of various diseases, including atherosclerosis, hypertension, diabetes, and cancer. LOX-1 is crucial in the pathogenesis of atherosclerosis and related cardiovascular diseases. It facilitates the uptake of ox-LDL by endothelial cells and macrophages, leading to foam cell formation and atherosclerotic plaque development. LOX-1 is involved in vascular inflammation and is a potential therapeutic target. Dyslipidemia, characterized by elevated lipid levels, can induce LOX-1 expression, contributing to atherosclerosis. LOX-1 is also linked to the renin-angiotensin system, which regulates blood pressure and cardiovascular disease pathogenesis. The interaction between LOX-1 and angiotensin II receptors reciprocally regulates their expression and activity. LOX-1 is involved in the formation of foam cells through the uptake of modified LDL. Factors such as proinflammatory cytokines, lipopolysaccharide, and high glucose levels can stimulate LOX-1 expression, leading to endothelial dysfunction and oxidative stress. LOX-1 is also implicated in the progression of atherosclerosis and thrombosis, with its expression being upregulated in conditions such as hypertension and diabetes. Therapeutic strategies targeting LOX-1, including pharmacological inhibitors and gene therapy, are being explored for the treatment of atherosclerosis and related diseases. Lifestyle modifications,LOX-1, or lectin-like oxidized low-density lipoprotein receptor 1, is a transmembrane glycoprotein that binds and internalizes oxidized low-density lipoprotein (ox-LDL) in foam cells. It is the main receptor for ox-LDL and belongs to the scavenger receptor family, which is associated with various cardiovascular diseases, particularly atherosclerosis. LOX-1 plays a critical role in the formation of atherosclerotic plaques in the endothelial intimal layer, which can evolve into complicated thrombi involving fibroblasts, activated platelets, apoptotic muscle cells, and macrophages transformed into foam cells. This process disrupts vascular endothelial homeostasis, leading to partial or total obstruction of blood vessels and potentially causing myocardial ischemia. LOX-1 is also involved in other pathologies such as obesity and diabetes mellitus. LOX-1 is a 50 kDa transmembrane glycoprotein that undergoes post-translational modifications, including N-glycosylation, which is essential for its function. It is expressed in macrophages, vascular smooth muscle cells, cardiomyocytes, platelets, and fibroblasts. LOX-1 has a secondary role in endothelial dysfunction and apoptosis. Mutations and polymorphisms in the LOX-1 gene can influence its function, with some variants, like LOXIN, potentially offering protective effects by blocking LOX-1 activation. LOX-1 is also involved in the development of various diseases, including atherosclerosis, hypertension, diabetes, and cancer. LOX-1 is crucial in the pathogenesis of atherosclerosis and related cardiovascular diseases. It facilitates the uptake of ox-LDL by endothelial cells and macrophages, leading to foam cell formation and atherosclerotic plaque development. LOX-1 is involved in vascular inflammation and is a potential therapeutic target. Dyslipidemia, characterized by elevated lipid levels, can induce LOX-1 expression, contributing to atherosclerosis. LOX-1 is also linked to the renin-angiotensin system, which regulates blood pressure and cardiovascular disease pathogenesis. The interaction between LOX-1 and angiotensin II receptors reciprocally regulates their expression and activity. LOX-1 is involved in the formation of foam cells through the uptake of modified LDL. Factors such as proinflammatory cytokines, lipopolysaccharide, and high glucose levels can stimulate LOX-1 expression, leading to endothelial dysfunction and oxidative stress. LOX-1 is also implicated in the progression of atherosclerosis and thrombosis, with its expression being upregulated in conditions such as hypertension and diabetes. Therapeutic strategies targeting LOX-1, including pharmacological inhibitors and gene therapy, are being explored for the treatment of atherosclerosis and related diseases. Lifestyle modifications,