Lipid transport processes play critically important roles in the development of atherosclerosis, a disease of accumulation of lipids within arterial walls. The interplay between lipid metabolism, transport, and deposition within the arterial wall is a critical contributor to the development and pathogenesis of this disease. Cholesterol is a key player in atherosclerosis. It is transported within the bloodstream by lipoproteins: low-density lipoprotein (LDL) and high-density lipoprotein (HDL). LDL cholesterol carries cholesterol from the liver to peripheral tissues, including the arterial wall. In contrast, HDL cholesterol transports cholesterol away from tissues to the liver for excretion from the body. Perturbation of these transport processes can lead to the accumulation of cholesterol-rich LDL particles in the arterial intima, initiating the formation of fatty streaks, a key early feature of atherosclerosis. Within the arterial intima, LDL particles undergo oxidative modifications that are triggered by factors including inflammation and oxidative stress. Such oxidative modifications make LDL particles more prone to aggregation, infiltration into the arterial wall, and interaction with immune cells. Oxidized LDL (oxLDL) is taken up by macrophages by receptor-mediated endocytosis together with phagocytosis, leading to the formation of foam cells. Macrophages have specific receptors (scavenger receptors) that recognize and bind to oxLDL, such as CD36, SR-A (scavenger receptor class A) and LOX-1 (lectin-like oxidized LDL receptor 1). When oxLDL binds to scavenger receptors, it triggers internalization of the oxLDL-receptor complex via endocytosis, bringing the oxLDL particles into the macrophage's cytoplasm. Once internalized, scavenged lipoproteins are transported to endosomes or lysosomes for degradation, with cholesteryl esters (CEs) hydrolysed by lysosomal acid lipase to unesterified free cholesterol (FC). FC is then transported to the ER, re-esterified by acyl-CoA: cholesterol acyltransferase 1 (ACAT) and stored as liquid droplets, generating macrophage’s foam-like appearance. Such foam cells contribute to the fatty streaks and plaque development observed in atherosclerosis. HDL plays a key role in the reverse cholesterol transport process, collecting excess cholesterol from peripheral tissues, including foam cells within atherosclerotic plaques. This “good” cholesterol is then transported back to the liver for excretion, a process that helps to mitigate plaque progression. Lipid accumulation within the arterial wall also triggers an inflammatory response as foam cells release inflammatory cytokines that contribute to plaque progression. Inflammatory mediators also promote the migration and proliferation of arterial smooth muscle cells (SMCs), which contribute to the fibrous cap overlying the plaque. Advanced atherosclerotic plaques can become unstable by accumulating a necrotic lipid-rich core, thinning of the fibrous cap, and inflammation. Plaque rupture exposes the highly thrombogenic core to the bloodstream, leading to blood clots (thrombosis) that can occlude blood flow. Lipid-lowering therapies, such as statins, reduce circulating LDL cholesterol. Statins inhibit HMG-CoA reductase in the liver, leading to reduced LDL levels and a decrease in atherosclerotic plaque formation. Additionally, novel therapies targeting lipid metabolism and transport pathways include inhibiting PCSK9, a protein that regulates the levels of LDL receptors on the surface of liver cells. Inhibitors lead to increased clearance of LDL cholesterol from the bloodstream. We offer a comprehensive product range of research reagents for studying lipid transport, including CD36 antibodies, ADFP antibodies, Apolipoprotein E antibodies, Apolipoprotein E ELISA Kits, and APOA4 ELISA Kits. Explore our full lipid transport product range below and discover more, for less.