Purpose of review
Lungs are extremely susceptible to injury, and despite advances in surgical management and immunosuppression, outcomes for lung transplantation
are the worst of any solid organ transplant. The success of lung transplantation
is limited by high rates of primary graft dysfunction
because of ischemia-reperfusion injury
characterized by robust inflammation
, alveolar damage, and vascular permeability. This review will summarize major mechanisms of lung ischemia-reperfusion injury
with a focus on the most recent findings in this area.
Over the past 18 months, numerous studies have described strategies to limit lung ischemia-reperfusion injury
in experimental settings, which often reveal mechanistic insight. Many of these strategies involved the use of various antioxidants, anti-inflammatory agents, mesenchymal stem cells, and ventilation with gaseous molecules. Further advancements have been achieved in understanding mechanisms of innate immune cell activation, neutrophil infiltration, endothelial barrier dysfunction, and oxidative stress responses.
Methods for prevention of primary graft dysfunction
after lung transplant are urgently needed, and understanding mechanisms of ischemia-reperfusion injury
is critical for the development of novel and effective therapeutic approaches. In doing so, both acute and chronic outcomes of lung transplant recipients will be significantly improved.