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.