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- W2103591331 endingPage "997" @default.
- W2103591331 startingPage "989" @default.
- W2103591331 abstract "Kidneys derived from brain death organ donors show an inferior survival when compared to kidneys derived from living donors. Brain death is known to induce organ injury by evoking an inflammatory response in the donor. Neuronal injury triggers an inflammatory response in the brain, leading to endothelial dysfunction and the release of cytokines in the circulation. Serum levels of interleukin-6, -8, -10, and monocyte chemoattractant protein-1 (MCP-1) are increased after brain death. Binding with cytokine-receptors in kidneys stimulates activation of nuclear factor-kappa B (NF-kappaB), selectins, adhesion molecules and production of chemokines leading to cellular influx. Mitogen-activated protein kinases (MAP-kinases) mediate inflammatory responses and together with NF-kappaB they seem to play an important role in brain death induced renal injury. Altering the activation state of MAP-kinases could be a promising drug target for early intervention to reduce cerebral injury related donor kidney damage and improve outcome after transplantation." @default.
- W2103591331 created "2016-06-24" @default.
- W2103591331 creator A5037152123 @default.
- W2103591331 creator A5076276339 @default.
- W2103591331 creator A5079070757 @default.
- W2103591331 date "2009-05-01" @default.
- W2103591331 modified "2023-10-14" @default.
- W2103591331 title "Signal Transduction Pathways Involved in Brain Death-Induced Renal Injury" @default.
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