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10.1038/s41420-018-0065-2 http://scihub22266oqcxt.onion/10.1038/s41420-018-0065-2 C6060103!6060103!30062051     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Discov 2018 ; 4 (ä): ä Nephropedia Template TP {{tp|p=30062051|t=2018. Autophagy activation contributes to lipid accumulation in tubular epithelial cells during kidney fibrosis |pdf=|usr=}}{{30062051}} gab.com Text Autophagy activation contributes to lipid accumulation in tubular epithelial cells during kidney fibrosis JO: Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=30062051 #FOAvip Sustained activation of autophagy and lipid accumulation in tubular epithelial cells (TECs) are both associated with the kidney fibrosis progression. Autophagy has been found involved in the lipid metabolism regulation through a bi-directional mechanism of inducing lipolysis as well as promoting lipid droplet formation. However, whether and how autophagy influences lipid accumulation in kidney fibrosis remain unclear. In the current study, we show that UUO-induced lipid accumulation in tubular cells was significantly reduced when the pharmacological inhibitor 3-MA or CQ was administrated both in vivo and in vitro. Of interest, colocalization of LDs and autophagosomes, as well as colocalization of LDs and lysosomes were undetected in UUO-induced fibrotic kidneys, although lysosome function remained robust, indicating the lipid accumulation is lipophagy-lysosome pathway independent. TGF-?1-induced lipid droplets formation in HK-2 cells were decreased when the Beclin-1 expression was silenced, implying that autophagy-upregulated lipid droplets formation is Beclin-1 dependent. Finally, CQ treatment of UUO-induced fibrotic kidneys reduced the expression of ?-SMA and tubular cell apoptosis and rescued the expression of E-cadherin, which was associated with the ameliorated lipid deposition. Therefore, our work documented that autophagy promotes lipid droplet formation in TECs in a Beclin-1-dependent manner, which causes renal lipotoxicity and contributes to the progression of kidney fibrosis. Twit Text FOAVip Autophagy activation contributes to lipid accumulation in tubular epithelial cells during kidney fibrosis ????Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=30062051 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30062051 #FOAvip English Wikipedia <ref>{{Cite pmid|30062051}}</ref> Autophagy activation contributes to lipid accumulation in tubular epithelial cells during kidney fibrosis #MMPMID30062051 Yan Q; Song Y; Zhang L; Chen Z; Yang C; Liu S; Yuan X; Gao H; Ding G; Wang H Cell Death Discov 2018[]; 4 (ä): ä PMID30062051show ga Sustained activation of autophagy and lipid accumulation in tubular epithelial cells (TECs) are both associated with the kidney fibrosis progression. Autophagy has been found involved in the lipid metabolism regulation through a bi-directional mechanism of inducing lipolysis as well as promoting lipid droplet formation. However, whether and how autophagy influences lipid accumulation in kidney fibrosis remain unclear. In the current study, we show that UUO-induced lipid accumulation in tubular cells was significantly reduced when the pharmacological inhibitor 3-MA or CQ was administrated both in vivo and in vitro. Of interest, colocalization of LDs and autophagosomes, as well as colocalization of LDs and lysosomes were undetected in UUO-induced fibrotic kidneys, although lysosome function remained robust, indicating the lipid accumulation is lipophagy-lysosome pathway independent. TGF-?1-induced lipid droplets formation in HK-2 cells were decreased when the Beclin-1 expression was silenced, implying that autophagy-upregulated lipid droplets formation is Beclin-1 dependent. Finally, CQ treatment of UUO-induced fibrotic kidneys reduced the expression of ?-SMA and tubular cell apoptosis and rescued the expression of E-cadherin, which was associated with the ameliorated lipid deposition. Therefore, our work documented that autophagy promotes lipid droplet formation in TECs in a Beclin-1-dependent manner, which causes renal lipotoxicity and contributes to the progression of kidney fibrosis. äAutophagy activation contributes to lipid accumulation in tubular epit(epmc).pdf DeepDyve Pubget Overpricing