Kidney transplantation represents the best treatment of end-stage renal disease. In addition to the degree of human leukocyte antigen matching, long-term graft survival is influenced by the quality of the graft before its transplantation. Quality criteria include the level of ischemic damage caused by the transplantation per se. Renal ischemic preconditioning (IP) consists of different approaches to prevent ischemia/reperfusion (I/R) damage induced by the interruption and recovery of renal circulation, as observed during transplantation. Distinct animal models show promising results regarding the efficiency of PCI to preserve kidney structure and function in I/R conditions. Characterizing the cellular cascades involved in I/R led to the identification of putative targets of renal IP, including the adenosine monophosphate-activated protein kinase (AMPK). AMPK is a ubiquitous energy sensor, which has been implicated in the maintenance of epithelial cell polarization under energy deprivation. Among others, the anti-diabetic drug, metformin, is a potent activator of AMPK. Here, we summarize the in vitro and in vivo data about the role of AMPK in renal IP. Defining the pharmacological conditions of IP would help to improve the quality of the renal graft before its transplantation, thereby increasing its long-term survival.
Keywords: AMP-activated protein kinase; Ischemic preconditioning; Kidney transplantation; Metformin; Metformine; Préconditionnement ischémique; Transplantation rénale.
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