Atherosclerosis is a cardiovascular disease characterized by the gradual accumulation of cholesterol, lipids, immune cells, and connective tissue within the walls of arteries. This condition ultimately leads to the formation of atherosclerotic plaques that can narrow and stiffen arteries, impairing blood flow and potentially triggering heart attacks or strokes. Whilst no single gene is solely responsible for atherosclerosis susceptibility, certain genetic variations are associated with an increased risk of developing the condition. Genetic variations in genes related to lipid metabolism and cholesterol regulation play a significant role in atherosclerosis risk. For example, apolipoprotein E gene variants (e.g., APOE ε4 allele) are associated with altered cholesterol metabolism and variations in the low-density lipoprotein receptor gene affect LDL cholesterol uptake and can impact atherosclerosis risk. Chronic inflammation contributes to atherosclerosis development and both interleukin-6 and tumour necrosis factor gene variants have been linked to atherosclerosis risk. Finally, large-scale genome-wide association studies (GWAS) have identified numerous additional genetic variants associated with atherosclerosis risk. Atherosclerosis begins with endothelial dysfunction triggered by inflammation. Inflammatory mediators including cytokines, reactive oxygen species (ROS), and chemokines are released in response to factors such as high blood pressure, smoking, and high cholesterol levels which damage the endothelium. Inflammation upregulates the expression of adhesion molecules on the inflamed endothelial cells, including vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin. These help leukocytes, including monocytes, adhere to the endothelial surface. In response to chemotactic signals produced by the inflamed endothelium, circulating monocytes are attracted to the site of inflammation. These monocytes are recruited from the bloodstream to the intima (innermost layer) of the arterial wall. Activated endothelial cells create gaps between them, allowing monocytes to migrate from the bloodstream into the subendothelial space, the area between the endothelium and the underlying layer of smooth muscle cells and extracellular matrix. Once within the arterial wall, monocytes differentiate into macrophages, key players in further promoting inflammation. LDL particles that have entered the arterial wall can be modified by oxidative stress and other processes. Oxidized LDL (OxLDL) particles are taken up by macrophages through scavenger receptors, particularly CD36 and SR-A1. The uptake of OxLDL transforms macrophages into so-called foam cells, which filled with lipid droplets. Foam cells are a hallmark of early atherosclerotic plaques. They accumulate within the intimal layer and are retained due to various factors, including inflammation-driven changes in the extracellular matrix and impaired reverse cholesterol transport. Accumulation of foam cells contribute to the formation of fatty streaks, the early stage of atherosclerotic lesions. As inflammation persists, smooth muscle cells migrate to the site and proliferate, leading to the formation of a fibrous cap over the fatty streak. Subsequent plaque rupture can then lead to blood clot formation (thrombosis) and sudden blockage of blood flow (e.g., heart attack or stroke). Plaque composition determines their stability, with plaques containing a larger lipid core and less fibrous tissue more likely to rupture, whilst mechanical forces generated by arterial pressure can stress the fibrous cap and potentially lead to rupture. We provide a large product catalogue of research tools for investigating atherosclerosis, including CD31 antibodies, TNF alpha antibodies, beta Catenin antibodies, TNF alpha ELISA Kits, and BDNF ELISA Kits. Explore our full atherosclerosis product range below and discover more, for less. Alternatively, you can explore our Vascular Inflammation, Diabetes Associated, and Lipoprotein Metabolism product ranges.