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A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/s41598-017-11829-2 http://scihub22266oqcxt.onion/10.1038/s41598-017-11829-2 C5596020!5596020 !28900259     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28900259 &cmd=llinks): Failed to open stream: HTTP request failed! 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Selective tubular activation of hypoxia-inducible factor-2? has dual effects on renal fibrosis |pdf=|usr=}}{{28900259 }} gab.com Text Selective tubular activation of hypoxia-inducible factor-2 has dual effects on renal fibrosis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28900259 #FOAvip Hypoxia-inducible factor (HIF) is a key transcriptional factor in the response to hypoxia. Although the effect of HIF activation in chronic kidney disease (CKD) has been widely evaluated, the results have been inconsistent until now. This study aimed to investigate the effects of HIF-2? activation on renal fibrosis according to the activation timing in inducible tubule-specific transgenic mice with non-diabetic CKD. HIF-2? activation in renal tubular cells upregulated mRNA and protein expressions of fibronectin and type 1 collagen associated with the activation of p38 mitogen-activated protein kinase. In CKD mice, activation of HIF-2? at the beginning of CKD significantly aggravated renal fibrosis, whereas it did not lead to renal dysfunction. However, activation at a late-stage of CKD abrogated both renal dysfunction and fibrosis, which was associated with restoration of renal vasculature and amelioration of hypoxia through increased renal tubular expression of VEGF and its isoforms. As with tubular cells with HIF-2? activation, those under hypoxia also upregulated VEGF, fibronectin, and type 1 collagen expressions associated with HIF-1? activation. In conclusion, late-stage renal tubular HIF-2? activation has protective effects on renal fibrosis and the resultant renal dysfunction, thus it could represent a therapeutic target in late stage of CKD. Twit Text FOAVip Selective tubular activation of hypoxia-inducible factor-2 has dual effects on renal fibrosis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28900259 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28900259 #FOAvip English Wikipedia <ref>{{Cite pmid|28900259 }}</ref> Selective tubular activation of hypoxia-inducible factor-2? has dual effects on renal fibrosis #MMPMID28900259 Kong KH ; Oh HJ ; Lim BJ ; Kim M ; Han KH ; Choi YH ; Kwon K ; Nam BY ; Park KS ; Park JT ; Han SH ; Yoo TH ; Lee S ; Kim SJ ; Kang DH ; Choi KB ; Eremina V ; Quaggin SE ; Ryu DR ; Kang SW Sci Rep 2017[Sep]; 7 (1 ): 11351 PMID28900259 show ga Hypoxia-inducible factor (HIF) is a key transcriptional factor in the response to hypoxia. Although the effect of HIF activation in chronic kidney disease (CKD) has been widely evaluated, the results have been inconsistent until now. This study aimed to investigate the effects of HIF-2? activation on renal fibrosis according to the activation timing in inducible tubule-specific transgenic mice with non-diabetic CKD. HIF-2? activation in renal tubular cells upregulated mRNA and protein expressions of fibronectin and type 1 collagen associated with the activation of p38 mitogen-activated protein kinase. In CKD mice, activation of HIF-2? at the beginning of CKD significantly aggravated renal fibrosis, whereas it did not lead to renal dysfunction. However, activation at a late-stage of CKD abrogated both renal dysfunction and fibrosis, which was associated with restoration of renal vasculature and amelioration of hypoxia through increased renal tubular expression of VEGF and its isoforms. As with tubular cells with HIF-2? activation, those under hypoxia also upregulated VEGF, fibronectin, and type 1 collagen expressions associated with HIF-1? activation. In conclusion, late-stage renal tubular HIF-2? activation has protective effects on renal fibrosis and the resultant renal dysfunction, thus it could represent a therapeutic target in late stage of CKD. |*Transcriptional Activation [MESH] |Animals [MESH] |Atrophy [MESH] |Basic Helix-Loop-Helix Transcription Factors/*genetics/metabolism [MESH] |Biomarkers [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Epithelial Cells/metabolism [MESH] |Fibrosis [MESH] |Glomerulonephritis, IGA/etiology/metabolism/pathology [MESH] |Humans [MESH] |Hypoxia/genetics/metabolism [MESH] |Kidney Diseases/*etiology/*metabolism/pathology [MESH] |Kidney Function Tests [MESH] |Kidney Tubules/*metabolism/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Transgenic [MESH]Selective tubular activation of hypoxia-inducible factor-2? has dual e(epmc).pdf DeepDyve Pubget Overpricing