The connections between lipoprotein metabolism and atherosclerosis underpin the disease's development and progression. Lipoproteins are the molecular complexes that transport lipids, including cholesterol and triglycerides, within the bloodstream, and dysregulation of their metabolism contributes to the accumulation of lipids within arterial walls, central to the pathogenesis of atherosclerosis. Low-density lipoprotein (LDL) particles are the primary carriers of cholesterol in the blood. High blood levels of LDL cholesterol are a major risk factor in atherosclerosis. LDL cholesterol is transported to peripheral tissues, including the arterial intima, where it can accumulate and undergo oxidative modifications. Oxidized LDL (oxLDL) is taken up by macrophages, leading to the formation of foam cells within the arterial wall, a hallmark of early atherosclerotic lesions. Conversely, High-density lipoprotein (HDL) particles participate in the reverse process and play a protective role against atherosclerosis. HDL carries excess cholesterol away from peripheral tissues, including from the foam cells in atherosclerotic plaques. This process, known as reverse cholesterol transport, prevents the build-up of cholesterol within the arterial wall and helps maintain plaque stability. Dyslipidaemia, characterized by abnormal levels of lipoproteins, contributes to inflammation occurring within the arterial wall. Elevated levels of LDL cholesterol and decreased levels of HDL cholesterol are associated with increased inflammation, which promotes the recruitment of immune cells to the intima and the progression of atherosclerosis. Very-low-density lipoprotein (VLDL) particles transport triglycerides synthesized in the liver to peripheral tissues. Elevated levels of VLDL and triglycerides are associated with atherosclerosis and cardiovascular risk. Triglyceride-rich particles can also contribute to the generation of smaller dense LDL particles that are more prone to oxidation and subsequent endocytosis by macrophages. Lipoprotein(a) (Lp(a)) is a lipoprotein that contains an LDL-like particle linked to a unique protein called apolipoprotein(a). Elevated levels of Lp(a) are associated with an increased risk of atherosclerosis and cardiovascular events. Lp(a) can interfere with the normal function of HDL, impairing reverse cholesterol transport and promoting inflammation. Moreover, Lp(a) is believed to interfere with the breakdown of blood clots, making plaques more prone to rupture and leading to the formation of thrombi (clots) that can cause heart attacks or strokes. Remnant lipoproteins, which include remnants of VLDL and chylomicrons (large lipoprotein particles that transport dietary triglycerides from the intestine) after they have delivered triglycerides to tissues, can also contribute to plaque formation. These remnants are enriched in cholesterol and can be taken up by macrophages in the arterial wall, promoting foam cell formation and inflammation. Apolipoproteins associate with lipoproteins and play key roles in their metabolism. For example, apolipoprotein B (apoB) is a component of both LDL and VLDL particles, and elevated levels of apoB are associated with an increased risk of atherosclerosis. Conversely, apolipoprotein A-I (apoA-I) is the major protein component of HDL and is critical for its anti-atherogenic properties. Understanding the connections between lipoprotein metabolism and atherosclerosis has led to the development of lipid-lowering therapies, such as statins, which reduce LDL cholesterol levels and decrease the risk of cardiovascular events. We offer a wide product range of research tools for studying lipoprotein metabolism, including LRP1 antibodies, COX2 antibodies, Phospholipase A2 antibodies, Angiotensinogen ELISA Kits, and 5 Lipoxygenase ELISA Kits. Explore our full lipoprotein metabolism product range below and discover more, for less.