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Ischemia-reperfusion injury is the tissue damage that occurs when blood supply returns to tissue after a period of ischemia or lack of oxygen. The absence of oxygen and nutrients during ischemia creates a condition where restoration of circulation results in inflammation and oxidative damage through induction of oxidative stress rather than (or along with) restoration of normal function. The pathophysiology involves multiple mechanisms including production of reactive oxygen species, inflammatory responses, microvascular injury with increased capillary permeability, and activation of various cell death pathways including apoptosis, necrosis, autophagy, and necroptosis. IRI is clinically significant in various conditions including myocardial infarction, stroke, organ transplantation, and limb injuries. Therapeutic approaches include pharmacological interventions, ischemic preconditioning, medical gases, vitamin therapy, and therapeutic hypothermia.
Reduction of reactive oxygen species, Inhibition of inflammatory mediators, Regulation of cell death pathways, Protection of mitochondrial function
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