Cell death and ischemia-reperfusion injury in lung transplantation

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-reperfu-sion in human lung transplants. Herein, we focus on the relationship between inflammation and pro-grammed 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 under -standing 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. (C) 2022 International Society for Heart and Lung Transplantation. All rights reserved.

Automated summary

This article discusses the relationship between cell death and inflammation caused by ischemia-reperfusion in lung transplantation. Different types of cell death and their related molecules are explored. The inhibition of cell death has been explored as a therapeutic approach for ischemia-reperfusion injury in lung transplantation. Understanding these mechanisms is important for donor management, organ preservation, and prevention and treatment of primary graft dysfunction during and after transplantation.