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10.1038/s41598-017-11049-8 http://scihub22266oqcxt.onion/10.1038/s41598-017-11049-8 C5593843!5593843 !28894140     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28894140 &cmd=llinks): Failed to open stream: HTTP request failed! 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D-serine, a novel uremic toxin, induces senescence in human renal tubular cells via GCN2 activation |pdf=|usr=}}{{28894140 }} gab.com Text D-serine, a novel uremic toxin, induces senescence in human renal tubular cells via GCN2 activation JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28894140 #FOAvip The prevalence of chronic kidney disease (CKD), characterized by progressive renal dysfunction with tubulointerstitial fibrosis, is increasing because of societal aging. Uremic toxins, accumulated during renal dysfunction, cause kidney damage, leading to renal deterioration. A recent metabolomic analysis revealed that plasma D-serine accumulation is associated with faster progression of renal dysfunction in CKD patients. However, the causal relationship and the underlying mechanisms remain unclear. Herein, we demonstrated that D-serine markedly induced cellular senescence and apoptosis in a human proximal tubular cell line, HK-2, and primary culture of human renal tubular cells. The former was accompanied by G2/M cell cycle arrest and senescence-associated secretory phenotype, including pro-fibrotic and pro-inflammatory factors, contributing to tubulointerstitial fibrosis. Integrated stress response mediated by the general control nonderepressible 2 played an important role in D-serine-induced tubular cell toxicity and pro-fibrotic phenotypes, accelerating CKD progression and kidney aging. D-serine upregulated the L-serine synthesis pathway. Furthermore, D-serine-induced suppression of tubular cell proliferation was ameliorated by L-serine administration, indicating that D-serine exposure induced an L-serine-deprived state in tubular cells, compensated by L-serine synthesis. Thus, this study unveils molecular mechanisms underlying D-serine-induced tubular damage and pro-fibrotic phenotypes, suggesting that D-serine is a uremic toxin involved in CKD pathogenesis. Twit Text FOAVip D-serine, a novel uremic toxin, induces senescence in human renal tubular cells via GCN2 activation ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28894140 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28894140 #FOAvip English Wikipedia <ref>{{Cite pmid|28894140 }}</ref> D-serine, a novel uremic toxin, induces senescence in human renal tubular cells via GCN2 activation #MMPMID28894140 Okada A ; Nangaku M ; Jao TM ; Maekawa H ; Ishimono Y ; Kawakami T ; Inagi R Sci Rep 2017[Sep]; 7 (1 ): 11168 PMID28894140 show ga The prevalence of chronic kidney disease (CKD), characterized by progressive renal dysfunction with tubulointerstitial fibrosis, is increasing because of societal aging. Uremic toxins, accumulated during renal dysfunction, cause kidney damage, leading to renal deterioration. A recent metabolomic analysis revealed that plasma D-serine accumulation is associated with faster progression of renal dysfunction in CKD patients. However, the causal relationship and the underlying mechanisms remain unclear. Herein, we demonstrated that D-serine markedly induced cellular senescence and apoptosis in a human proximal tubular cell line, HK-2, and primary culture of human renal tubular cells. The former was accompanied by G2/M cell cycle arrest and senescence-associated secretory phenotype, including pro-fibrotic and pro-inflammatory factors, contributing to tubulointerstitial fibrosis. Integrated stress response mediated by the general control nonderepressible 2 played an important role in D-serine-induced tubular cell toxicity and pro-fibrotic phenotypes, accelerating CKD progression and kidney aging. D-serine upregulated the L-serine synthesis pathway. Furthermore, D-serine-induced suppression of tubular cell proliferation was ameliorated by L-serine administration, indicating that D-serine exposure induced an L-serine-deprived state in tubular cells, compensated by L-serine synthesis. Thus, this study unveils molecular mechanisms underlying D-serine-induced tubular damage and pro-fibrotic phenotypes, suggesting that D-serine is a uremic toxin involved in CKD pathogenesis. |Aging/*drug effects [MESH] |Apoptosis [MESH] |Cell Cycle Checkpoints [MESH] |Cells, Cultured [MESH] |Epithelial Cells/*drug effects/pathology [MESH] |Humans [MESH] |Kidney Diseases/*physiopathology [MESH] |Kidney Tubules, Proximal/*drug effects/pathology [MESH] |Protein Serine-Threonine Kinases/*metabolism [MESH]D-serine, a novel uremic toxin, induces senescence in human renal tubu(epmc).pdf DeepDyve Pubget Overpricing