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10.1038/srep26954 http://scihub22266oqcxt.onion/10.1038/srep26954 C4887891!4887891 !27246399     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27246399 &cmd=llinks): Failed to open stream: HTTP request failed! 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Pharmacological inhibition of MyD88 homodimerization counteracts renal ischemia reperfusion-induced progressive renal injury in vivo and in vitro |pdf=|usr=}}{{27246399 }} gab.com Text Pharmacological inhibition of MyD88 homodimerization counteracts renal ischemia reperfusion-induced progressive renal injury in vivo and in vitro JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27246399 #FOAvip The activation of innate immunity via myeloid differentiation factor 88 (MyD88) contributes to ischemia reperfusion (I/R) induced acute kidney injury (AKI) and chronic kidney injury. However, since there have not yet been any effective therapy, the exact pharmacological role of MyD88 in the prevention and treatment of renal ischemia reperfusion injury (IRI) is not known. We designed a small molecular compound, TJ-M2010-2, which inhibited MyD88 homodimerization. We used an established unilateral I/R mouse model. All mice undergoing 80?min ischemia through uninephrectomy died within five days without intervention. However, treatment with TJ-M2010-2 alone significantly improved the survival rate to 58.3%. Co-treatment of TJ-M2010-2 with the CD154 antagonist increased survival rates up to 100%. Twenty-eight days post-I/R of 60?min ischemia without nephrectomy, TJ-M2010-2 markedly attenuated renal interstitial and inhibited TGF-?1-induced epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Furthermore, TJ-M2010-2 remarkably inhibited TLR/MyD88 signaling in vivo and in vitro. In conclusion, our findings highlight the promising clinical potential of MyD88 inhibitor in preventing and treating acute or chronic renal I/R injuries, and the therapeutic functionality of dual-system inhibition strategy in IRI-induced AKI. Moreover, MyD88 inhibition ameliorates renal I/R injury-induced tubular interstitial fibrosis by suppressing EMT. Twit Text FOAVip Pharmacological inhibition of MyD88 homodimerization counteracts renal ischemia reperfusion-induced progressive renal injury in vivo and in vitro ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27246399 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27246399 #FOAvip English Wikipedia <ref>{{Cite pmid|27246399 }}</ref> Pharmacological inhibition of MyD88 homodimerization counteracts renal ischemia reperfusion-induced progressive renal injury in vivo and in vitro #MMPMID27246399 Zhang LM ; Liu JH ; Xue CB ; Li MQ ; Xing S ; Zhang X ; He WT ; Jiang FC ; Lu X ; Zhou P Sci Rep 2016[Jun]; 6 (ä): 26954 PMID27246399 show ga The activation of innate immunity via myeloid differentiation factor 88 (MyD88) contributes to ischemia reperfusion (I/R) induced acute kidney injury (AKI) and chronic kidney injury. However, since there have not yet been any effective therapy, the exact pharmacological role of MyD88 in the prevention and treatment of renal ischemia reperfusion injury (IRI) is not known. We designed a small molecular compound, TJ-M2010-2, which inhibited MyD88 homodimerization. We used an established unilateral I/R mouse model. All mice undergoing 80?min ischemia through uninephrectomy died within five days without intervention. However, treatment with TJ-M2010-2 alone significantly improved the survival rate to 58.3%. Co-treatment of TJ-M2010-2 with the CD154 antagonist increased survival rates up to 100%. Twenty-eight days post-I/R of 60?min ischemia without nephrectomy, TJ-M2010-2 markedly attenuated renal interstitial and inhibited TGF-?1-induced epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Furthermore, TJ-M2010-2 remarkably inhibited TLR/MyD88 signaling in vivo and in vitro. In conclusion, our findings highlight the promising clinical potential of MyD88 inhibitor in preventing and treating acute or chronic renal I/R injuries, and the therapeutic functionality of dual-system inhibition strategy in IRI-induced AKI. Moreover, MyD88 inhibition ameliorates renal I/R injury-induced tubular interstitial fibrosis by suppressing EMT. |Animals [MESH] |Antibodies, Monoclonal/*pharmacology [MESH] |Binding Sites [MESH] |CD40 Ligand/*antagonists & inhibitors/genetics/immunology [MESH] |Drug Design [MESH] |Drug Therapy, Combination [MESH] |Epithelial Cells/drug effects/immunology/pathology [MESH] |Epithelial-Mesenchymal Transition/drug effects [MESH] |Gene Expression [MESH] |Immunity, Innate/drug effects [MESH] |Kidney/drug effects/immunology/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH] |Molecular Docking Simulation [MESH] |Myeloid Differentiation Factor 88/*antagonists & inhibitors/genetics/immunology [MESH] |Piperazines/*pharmacology [MESH] |Protein Binding [MESH] |Protein Conformation, alpha-Helical [MESH] |Protein Conformation, beta-Strand [MESH] |Protein Interaction Domains and Motifs [MESH] |Protein Multimerization/drug effects [MESH] |Reperfusion Injury/genetics/immunology/mortality/*prevention & control [MESH] |Survival Analysis [MESH]Pharmacological inhibition of MyD88 homodimerization counteracts renal(epmc).pdf DeepDyve Pubget Overpricing