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• W1763518723 abstract "Received: December 6, 2010 , Accepted: December 25, 2010 , Published: December 25, 2010 // Ischemia-reperfusion injury induces intense inflammatory response and tissue damages resulting from the capacity of endogenous constituents called damageassociated molecular patterns (DAMPs) released by damaged or necrotic cells, to activate signaling pathways mediated by receptors of the innate immune systems. Among them, two members of the Toll-like receptors (TLR) family, TLR2 and TLR4 have been shown to play key roles in the induction of inflammatory response and cell apoptosis in a variety of ischemic tissues. The oxidative stress injury caused by I/R injury has been attributed to the activation of MAP kinase pathways, including those of ERK, JNK and p38. Here, we summarise recent findings concerning the role of the protein phosphatase 5 involved in the selective regulation of TLR2-mediated ERK1/2 signaling and the identification of the key role of the non-phagocytic NADPH oxidase 4 producing reactive oxygen species in the control of TLR4-mediated apoptosis in murine models of renal I/R injury and in post-hypoxic kidney tubule cells. The identification of molecules signaling involved in the ER stress-induced apoptotic signaling cascade may therefore represent potential targets to prevent the induction of apoptosis in hypoxic tissues. &nbsp" @default.
• W1763518723 created "2016-06-24" @default.
• W1763518723 creator A5001091431 @default.
• W1763518723 creator A5001718959 @default.
• W1763518723 creator A5089949394 @default.
• W1763518723 date "2010-12-25" @default.
• W1763518723 modified "2023-10-02" @default.
• W1763518723 title "Differential activation of Toll-like receptor-mediated apoptosis induced by hypoxia" @default.
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• W1763518723 doi "https://doi.org/10.18632/oncotarget.209" @default.
• W1763518723 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3157738" @default.
• W1763518723 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21321383" @default.
• W1763518723 hasPublicationYear "2010" @default.
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