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Cell death and ischemia-reperfusion injury in lung transplantation.

Abstract
Lung transplantation is the most effective therapy for patients with end-stage lung disease. However, concern of donor lung damage and ischemia-reperfusion induced lung injury limits the use of "marginal" donor lungs. Recent transcriptomic studies have demonstrated that the enrichment of gene-clusters related to cell death and inflammation are the most profound signals during ischemia-reperfusion in human lung transplants. Herein, we focus on the relationship between inflammation and programmed cell death, especially necroptosis, mitochondrial permeability transition-initiated regulated necrosis, pyroptosis, ferroptosis, and autophagic cell death. Cell death-related molecules have been tested as potential biomarkers for donor lung assessment. Inhibitors for various types of cell death have been explored as therapeutics for ischemia reperfusion injury in lung transplantation. A deeper understanding of these mechanisms may help to improve donor management, organ preservation, prevention and treatment of primary graft dysfunction during and post transplantation. Moreover, evaluation and treatment of cell death and inflammation during ex vivo lung perfusion may be a game changer in donor organ management, assessment, repair, and reconditioning.
AuthorsMegan Capuzzimati, Olivia Hough, Mingyao Liu
JournalThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation (J Heart Lung Transplant) Vol. 41 Issue 8 Pg. 1003-1013 (08 2022) ISSN: 1557-3117 [Electronic] United States
PMID35710485 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2022 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.
Topics
  • Cell Death
  • Humans
  • Inflammation (etiology)
  • Lung
  • Lung Transplantation (adverse effects)
  • Perfusion (adverse effects)
  • Reperfusion Injury (prevention & control)

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