Ischemia reperfusion injury (IRI), one of the key problems in clinical transplantation, is an inevitable consequence of organ procurement and implantation procedure. There are two major stages of IRI with distinct mechanisms of tissue damage: loss of blood supply to the organ, and alterations in local pH, glycogen consumption, and adenosine triphosphate (ATP) depletion. Organ injury is perpetuated by the release of pro-inflammatory cytokines and activation of innate immune cells. The innate immune sensors (Toll-like receptors, RIG-I-like receptor, nucleotide-binding domain-like receptor) are involved in ischemia reperfusion injury. IRI is an inevitable consequence of organ procurement and implantation procedure. The chapter also discusses the current understanding of IRI in immune activation, as well as the conversion of an immunologically quiescent organ to a highly inflammatory one. Identification of new molecular pathways (Tim-1/4, inflammasome) provides targets for new drugs to reduce organ damage.
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