Thrombosis is a critical life-threatening event in atherosclerosis. The molecular processes underlying thrombosis in the context of atherosclerosis involve interactions between blood components, cells, and the disrupted arterial wall within atherosclerotic plaques. Atherosclerosis begins with the accumulation of lipids and inflammatory cells within the arterial intima. This process triggers local endothelial dysfunction, leading to reduced production of nitric oxide (NO), a molecule that helps both to maintain the dilation of blood vessels and inhibit platelet aggregation. The dysfunctional arterial endothelium also expresses adhesion molecules that attract platelets and immune cells to the site of plaque formation. As the endothelium becomes activated, platelets begin to adhere to the exposed subendothelial matrix and undergo activation. The adhesion of platelets to collagen and von Willebrand factor (vWF) triggers platelet shape change, granule release, and the exposure of platelet receptors such as P-selectin and GPIIb/IIIa. Activated platelets then release ADP and thromboxane A2, which further stimulate platelet aggregation and recruitment. The disrupted endothelium exposes tissue factor, which initiates the coagulation cascade. Tissue factor (also known as factor III) plays a critical role in the blood coagulation cascade. It is a transmembrane protein found on the surface of cells, particularly cells lining blood vessels and cells in various tissues. Tissue factor is essential for initiating the extrinsic pathway of the blood coagulation cascade, which ultimately leads to the formation of blood clots. Tissue factor interacts with circulating factor VII, leading to the activation of a series of clotting factors and ultimately the formation of thrombin, a key protease that converts fibrinogen to fibrin, which forms the meshwork of a blood clot. Thrombin cleaves fibrinogen generating fibrin monomers, which can self-assemble into a stable fibrin network. This network subsequently entraps platelets, red blood cells, and other blood components, forming a blood clot or thrombus. The clotting cascade thus amplifies this process through positive feedback loops. In advanced atherosclerotic plaques, inflammation, oxidative stress, and enzymatic degradation weaken the fibrous cap covering the lipid-rich core. Plaque rupture exposes thrombogenic material, such as tissue factor, collagen, and lipids, to the bloodstream. Platelets then adhere to the disrupted plaque surface and aggregate, initiating thrombosis. The clot can obstruct blood flow, leading to tissue ischemia and potential downstream complications. Inflammation within the plaque also contributes to thrombosis. Immune cells, such as macrophages, can release tissue factor, cytokines, and proteases that promote coagulation. Inflammatory mediators can therefore amplify platelet activation and endothelial dysfunction, further facilitating thrombosis. The body maintains a balance between pro-thrombotic and anti-thrombotic factors to prevent excessive clotting. Endothelial cells normally produce anti-thrombotic molecules, such as prostacyclin and tissue plasminogen activator (tPA), which counteract clot formation. However, in the context of atherosclerosis, this balance is disrupted, favouring thrombosis. We provide a wide product catalogue of research tools for studying thrombosis, including MMP9 antibodies, MMP3 antibodies, Cystatin C antibodies, BDNF ELISA Kits, and MMP3 ELISA Kits. Explore our full thrombosis product range below and discover more, for less. Alternatively, you can explore our Endothelial Mediators & Regulators, Fibrinolysis, and Platelets product ranges.