Heme Oxygenase-1 (HO-1)

Transplantation is considered one of the most effective ways to overcome terminal dysfunction and failure of some organs. By transplanting organs or tissues between two genetically distinct individuals, an immune mediated response is triggered in the transplant recipient that evokes a potent inflammatory reaction, causing cell injury/death and leading to graft dysfunction and rejection. So far the main therapeutic strategy used to maintain graft function and survival has been to modulate the host immune response directed against the transplanted organ. In the case of an immediately vascularized transplant, the endothelial cell (EC) monolayer lining the blood vessels of the graft acts as the first target of the anti-graft immune response. We have suggested that the survival of grafts may relay on how these cells react to the anti-graft immune response: whether in a rejection-promoting or a “protective”