Graft coronary artery disease continues to obstruct the long-term success of heart transplantation. Although antigen-dependent factors play a central role, more recent data indicate the importance of antigen-independent events in this disease process. In particular, the obligatory oxidative stress that cardiac allografts incur with ischemia and reperfusion appears to be associated with later graft function and the development of vasculopathy. This review provides evidence for this link, highlights some of the molecular events in this process, and points toward therapies that may benefit heart transplant recipients in the future.
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