Vascular inflammation is a key process in the development and progression of atherosclerosis of arterial walls. The events underlying vascular inflammation involve interactions between immune cells, endothelial cells, cytokines, chemokines, and adhesion molecules, collectively contributing to the initiation and progression of atherosclerosis. Vascular inflammation begins with endothelial dysfunction, whereby endothelial cells lining the inner surface of blood vessels become activated in response to high blood pressure, oxidative stress, or LDL cholesterol. Activated endothelial cells respond to damage by upregulating the expression of specific adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Such adhesion molecules on activated endothelial cells facilitate the rolling, adhesion, and transmigration of circulating immune cells, particularly monocytes, to the subendothelial space. Monocytes are attracted by chemokines released by endothelial cells and other immune cells. For example, Monocyte Chemoattractant Protein-1 (MCP-1, CCL2) and Macrophage Inflammatory Protein-1 alpha (MIP-1α, CCL3) are key chemokines involved in the recruitment of monocytes by damaged endothelial cells to the inflamed arterial wall. MCP-1 binds to its receptor, CCR2 (C-C chemokine receptor 2) expressed on the surface of monocytes, triggering a signalling process that leads to monocyte activation, adhesion to the endothelium, and subsequent migration into the arterial intima (inner layer). Monocytes that have transmigrated into the subendothelial space differentiate into macrophages within the atherosclerotic plaque upon exposure to factors that include Macrophage Colony-Stimulating Factor (M-CSF) produced by endothelial cells. Macrophages engulf oxidized LDL cholesterol, forming foam cells. This process is therefore a key early event in atherosclerosis, leading to the development of fatty streaks and the progression of plaques. Activated macrophages also release pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and tumour necrosis factor-alpha (TNF-α), which further amplify the inflammatory response, further promoting endothelial dysfunction, activating vascular smooth muscle cells, and stimulating further immune cell recruitment. Inflammatory mediators released by immune cells also stimulate the migration and proliferation of vascular smooth muscle cells (VSMCs) from the media to the intima of the arterial wall. VSMCs contribute to the formation of the fibrous caps overlying lipid-rich plaques. However, excessive VSMC proliferation can lead to vessel narrowing and plaque instability. Inflammation within the plaque leads to the generation of reactive oxygen species (ROS) by various cell types, including macrophages and VSMCs. ROS causes oxidative stress, damaging lipids, proteins, and DNA within the arterial wall. Oxidative stress thus perpetuates the inflammatory response and further promotes lipid oxidation, central to plaque progression. Vascular inflammation thus creates positive feedback loops, amplifying the initial inflammatory response. Immune cells attract more immune cells, cytokines activate additional cells, and inflammation contributes to the further activation of endothelial cells and vascular smooth muscle cells. Chronic vascular inflammation also promotes the weakening and potentially dangerous destabilization of atherosclerotic plaques. Inflammatory factors weaken the fibrous cap, increasing the risk of plaque rupture, exposing the plaque’s thrombogenic material to the bloodstream, triggering thrombosis and acute cardiovascular events. We offer a comprehensive product catalogue of research tools for studying vascular inflammation, including CD31 antibodies, TNF alpha antibodies, beta Catenin antibodies, TNF alpha ELISA Kits, and ICAM1 ELISA Kits. Explore our full vascular inflammation product range below and discover more, for less. Alternatively, you can explore our Leukocyte Recruitment, Inflammatory Mediators, and Innate & Adaptive Immunity product ranges.