In solid organ transplantation, ischemia/reperfusion (IR) injury during organ procurement, storage and reperfusion is an unavoidable detrimental event for the graft, as it amplifies graft inflammation and rejection. Intracellular mitogen-activated protein kinase (MAPK) signaling pathways regulate inflammation and cell survival during IR injury. The four best-characterized MAPK subfamilies are the c-Jun NH2-terminal kinase (JNK), extracellular signal- regulated kinase-1/2 (ERK1/2), p38 MAPK, and big MAPK-1 (BMK1/ERK5). Here, we review the role of MAPK activation during myocardial IR injury as it occurs during heart transplantation. Most of our current knowledge regarding MAPK activation and cardioprotection comes from studies of preconditioning and postconditioning in nontransplanted hearts. JNK and p38 MAPK activation contributes to myocardial IR injury after prolonged hypothermic storage. p38 MAPK inhibition improves cardiac function after cold storage, rewarming and reperfusion. Small-molecule p38 MAPK inhibitors have been tested clinically in patients with chronic inflammatory diseases, but not in transplanted patients, so far. Organ transplantation offers the opportunity of starting a preconditioning treatment before organ procurement or during cold storage, thus modulating early events in IR injury. Future studies will need to evaluate combined strategies including p38 MAPK and/or JNK inhibition, ERK1/2 activation, pre- or postconditioning protocols, new storage solutions, and gentle reperfusion. 1. Introduction Heart transplantation is the final therapeutic option for heart failure [1]. Over the past two decades, advances in immunosuppression and antimicrobial agents have improved outcomes after heart transplantation. An analysis of the UNOS database in 14,401 first-time orthotopic heart transplant recipients between the years 1999 and 2006 showed that the survival rate at 30 days, 1 year, and 5 years was 94%, 87%, and 75%, respectively, for the young group (<60 years of age) and 93%, 84%, and 69% for the older group [2]. Graft vasculopathy, a unique form of accelerated coronary artery disease, is a major cause of late graft failure [3]. The disease is characterized by intimal thickening mainly due to smooth muscle cell proliferation and fibrosis. Occlusive narrowing of the coronary vessels can develop within a few months and is not prevented by current treatments. The pathogenesis of graft vasculopathy is complex and has been reviewed elsewhere [4–6]. The observation that, while graft coronary arteries develop lesions, the host’s native arteries
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