“…Secondly, reactive oxygen species generated by an influx of cytosolic calcium during warm and cold ischemic times in response to ATP generation creates a cycle of inflammatory changes and eventual endothelial damage, which leads to more inflammation from increased capillary permeability and cytokine release, ultimately leading to cell death in the donor allograft ( 6 , 7 ). Furthermore, the milieu of donor and recipient risk factors, which we will discuss in this article, are also key in the pathophysiology of PGD ( 8 , 9 ). Importantly, PGD is strongly associated with the development of chronic lung allograft dysfunction (CLAD), which is the primary cause of long-term morbidity and mortality after LTx ( 10 , 11 ).…”