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Lukenaite, B; Griciune, E; Leber, B; Strupas, K; Stiegler, P; Schemmer, P.
Necroptosis in Solid Organ Transplantation: A Literature Overview.
Int J Mol Sci. 2022; 23(7): Doi: 10.3390/ijms23073677 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz
Stiegler Philipp
Co-Autor*innen der Med Uni Graz
Leber Bettina
Schemmer Peter

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Ischemia-reperfusion injury (IRI) is encountered in various stages during solid organ transplantation (SOT). IRI is known to be a multifactorial inflammatory condition involving hypoxia, metabolic stress, leukocyte extravasation, cellular death (including apoptosis, necrosis and necroptosis) and an activation of immune response. Although the cycle of sterile inflammation during IRI is consistent among different organs, the underlying mechanisms are poorly understood. Receptor-interacting protein kinase 3 (RIPK3) and mixed-lineage kinase domain-like pseudokinase (MLKL) are thought to be crucial in the implementation of necroptosis. Moreover, apart from "silent" apoptotic death, necrosis also causes sterile inflammation-necroinflammation, which is triggered by various damage-associated molecular patterns (DAMPs). Those DAMPs activate the innate immune system, causing local and systemic inflammatory responses, which can result in graft failure. In this overview we summarize knowledge on mechanisms of sterile inflammation processes during SOT with special focus on necroptosis and IRI and discuss protective strategies.
Find related publications in this database (using NLM MeSH Indexing)
Apoptosis - physiology
Humans - administration & dosage
Inflammation - metabolism
Necroptosis - administration & dosage
Necrosis - administration & dosage
Organ Transplantation - adverse effects
Receptor-Interacting Protein Serine-Threonine Kinases - metabolism
Reperfusion Injury - metabolism

Find related publications in this database (Keywords)
ischemia-reperfusion injury
solid organ transplantation
sterile inflammation
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