Ischemia-reperfusion injury (IRI) is a phenomenon in which blood flow to a tissue or organ is temporarily reduced or completely interrupted (ischemia) and subsequently restored (reperfusion). Whilst reperfusion is essential to restore oxygen and nutrients, it can lead to additional tissue damage. IRI is particularly relevant in the context of atherosclerosis due to its roles in exacerbating tissue damage and influencing the progression of the disease. During ischemia, reduced blood flow deprives affected cells of oxygen and nutrients, leading to a temporary shift from aerobic to anaerobic metabolism. This however results in the accumulation of metabolic by-products and the depletion of ATP, compromising cellular functions. When blood flow is restored, resupply of oxygen and nutrients triggers a series of molecular responses that collectively contribute to reperfusion injury: Reperfusion firstly introduces a sudden influx of molecular oxygen, which leads to the rapid generation of excessive ROS through the process of oxidative phosphorylation. ROS, such as superoxide anions and hydrogen peroxide, causes oxidative stress, damaging lipids, proteins, and DNA within cells. In atherosclerosis, ROS is known to contribute to endothelial dysfunction, inflammation, and lipid oxidation, all of which play pivotal roles in plaque formation and progression. Reperfusion also initiates an inflammatory response, characterized by the activation of immune cells like neutrophils and macrophages. These cells then release pro-inflammatory cytokines and chemokines, further contributing to tissue damage. In atherosclerosis, inflammation is known driver of plaque development and instability, as immune cells infiltrate plaques and release enzymes that weaken the fibrous cap, increasing the risk of rupture. The sudden restoration of blood flow by reperfusion can also disrupt the fragile endothelial layer, leading to endothelial dysfunction. Dysfunction compromises the release of vasodilators, such as nitric oxide, and increases the expression of adhesion molecules that can then attract immune cells, promoting inflammation. In atherosclerosis, endothelial dysfunction is a central event that contributes to the initiation and progression of plaques, promoting the adhesion of monocytes and the accumulation of lipids. Ischemia also reduces the ability of cells to maintain their calcium ion balance. Ischemia can disrupt calcium ion flux by causing mitochondrial dysfunction, reducing ATP levels, promoting excitotoxicity, or compromising membrane integrity. Upon reperfusion, an excessive influx of calcium ions occurs, leading to cellular damage. Excessive calcium levels can lead to the opening of the mitochondrial permeability transition pore (mPTP), which disrupts the mitochondrial membrane potential and causes mitochondrial swelling. This, in turn, impairs ATP production and triggers the release of pro-apoptotic factors, contributing to cell death. In atherosclerosis, calcium overload can therefore exacerbate inflammation, cell death, and plaque instability. Finally, reperfusion can trigger various forms of cell death, including apoptosis and necrosis, due to the accumulation of oxidative stress and calcium overload. In atherosclerosis, cell death contributes to the formation of the necrotic cores present within plaques, rendering them vulnerable to rupture. Whilst IRI primarily occurs during events like heart attacks and strokes, it has downstream effects that can exacerbate the molecular processes associated with atherosclerotic plaque development, progression, and rupture, causing further cardiovascular damage. We offer a large product catalogue of research reagents for investigating ischemia and reperfusion, including Hsp27 antibodies, Thymidine Phosphorylase antibodies, EPO Receptor antibodies, Hsp27 ELISA Kits, and EPO Receptor ELISA Kits. Explore our full ischemia and reperfusion product range below and discover more, for less.