Ischemia and reperfusion injury

Yuan Zhai, Yoichiro Uchida, Bibo Ke, Haofeng Ji, Jerzy W. Kupiec-Weglinski

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

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.

Original languageEnglish
Title of host publicationTransplant Immunology
PublisherWiley-Blackwell
Pages128-141
Number of pages14
ISBN (Electronic)9781119072997
ISBN (Print)9780470658215
DOIs
Publication statusPublished - 12-09-2015
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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