Diabetes-associated atherosclerosis involves multiple molecular mechanisms contributing to the development and progression of atherosclerotic plaques in individuals with diabetes mellitus. Diabetes is considered a major independent risk factor for atherosclerosis and plays a significant role in accelerating the progression of the disease. The degree of risk varies based on several factors, including the type of diabetes, glycaemic control, and other associated risk factors. Several factors contribute to the relationship between diabetes and increased risk of atherosclerosis. Insulin resistance, a hallmark of type 2 diabetes, initially leads to elevated blood glucose levels (hyperglycaemia). Elevated glucose levels can then lead to an increased flux of glucose through metabolic pathways, particularly in mitochondria, with increased metabolic activity overwhelming the mitochondrial electron transport chain (ETC), leading to electron leakage, and increased reactive oxygen species (ROS) generation. Additionally, excess glucose can also be shunted through the polyol pathway which consumes NADPH, a key cofactor for antioxidant enzymes. Together, increased ROS and reduced antioxidant capacity increase oxidative stress which can damage endothelial cells potentially leading to apoptosis, and can reduce nitric oxide bioavailability (a vasodilator), and promote inflammation. Hyperglycaemia also leads to the production of advanced glycation end products (AGEs) such as Nε-(carboxymethyl)lysine (CML) and Nε-(carboxyethyl)lysine (CEL) which can bind to their receptors (RAGE) on endothelial cells and immune cells. RAGE is the primary cell surface receptor that interacts with AGEs and is a multi-ligand receptor belonging to the immunoglobulin superfamily and expressed on endothelial cells, immune cells, smooth muscle cells, and macrophages. In the context of atherosclerosis, RAGE activation by AGEs is thought to contribute to inflammation, oxidative stress, and endothelial dysfunction, leading to further intracellular ROS generation and inflammation. For example, binding of AGEs to RAGE on macrophages can trigger the production of pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-α), amplifying the local inflammatory response within the plaque, and can enhance foam cell formation and thereby contribute to the progression of the plaque. Collectively, such effects can cause cellular damage within the arterial walls, thereby promoting atherosclerosis. Diabetes also triggers a chronic low-grade inflammatory state, characterized by elevated levels of inflammatory cytokines such as interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α). These cytokines stimulate the recruitment of immune cells, including monocytes, to the arterial wall. Monocytes can differentiate into macrophages, engulf lipids, and become foam cells, contributing to the formation of fatty streaks and early atherosclerotic lesions. Diabetes-associated atherosclerosis also tends to feature plaques with distinct physical characteristics, including larger necrotic cores, thinner fibrous caps, and increased inflammation. These features render the plaques more susceptible to subsequent rupture, which can lead to thrombosis and acute cardiovascular events. Finally, in both type 1 and type 2 diabetes, hyperinsulinemia (excess insulin in the blood) can occur due to impaired insulin utilization. Elevated insulin levels can stimulate the growth of smooth muscle cells (SMCs) within the arterial wall, contributing to the thickening of the intima and subsequent plaque formation. We offer a wide product catalogue of research reagents for studying diabetes-associated atherosclerosis, including IRS1 antibodies, RBP4 antibodies, Insulin antibodies, BDNF ELISA Kits, and Leptin ELISA Kits. Explore our full diabetes-associated atherosclerosis product range below and discover more, for less.