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10.1038/s41598-018-29417-3 http://scihub22266oqcxt.onion/10.1038/s41598-018-29417-3 C6054654!6054654!30030497     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2018 ; 8 (ä): ä Nephropedia Template TP {{tp|p=30030497|t=2018. A blockade of PI3K? signaling effectively mitigates angiotensin II-induced renal injury and fibrosis in a mouse model |pdf=|usr=}}{{30030497}} gab.com Text A blockade of PI3K signaling effectively mitigates angiotensin II-induced renal injury and fibrosis in a mouse model JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=30030497 #FOAvip Chronic kidney disease (CKD) poses a formidable challenge for public healthcare worldwide as vast majority of patients with CKD are also at risk of accelerated cardiovascular disease and death. Renal fibrosis is the common manifestation of CKD that usually leads to end-stage renal disease although the molecular events leading to chronic renal fibrosis and eventually chronic renal failure remain to be fully understood. Nonetheless, emerging evidence suggests that an aberrant activation of PI3K? signaling may play an important role in regulating profibrotic phenotypes. Here, we investigate whether a blockade of PI3K? signaling exerts any beneficial effect on alleviating kidney injury and renal fibrosis. Using a mouse model of angiotensin II (Ang II)-induced renal damage, we demonstrate that PI3K? inhibitor AS605240 effectively mitigates Ang II-induced increases in serum creatinine and blood urea nitrogen, renal interstitial collagen deposition, the accumulation of ECM proteins and the expression of ?-Sma and fibrosis-related genes in vivo. Mechanistically, we reveal that AS605240 effectively inhibits Ang II-induced cell proliferation and phosphorylation of Akt in fibroblast cells. Furthermore, we demonstrate that Ang II-upregulated expression of IL-6, Tnf-?, IL-1? and Tgf-?1 is significantly attenuated in the mice treated with AS605240. Taken together, our results demonstrate that PI3K? may function as a critical mediator of Ang II-induced renal injury and fibrosis. It is thus conceivable that targeted inhibition of PI3K? signaling may constitute a novel therapeutic approach to the clinical management of renal fibrosis, renal hypertension and/or CKD. Twit Text FOAVip A blockade of PI3K signaling effectively mitigates angiotensin II-induced renal injury and fibrosis in a mouse model ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=30030497 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30030497 #FOAvip English Wikipedia <ref>{{Cite pmid|30030497}}</ref> A blockade of PI3K? signaling effectively mitigates angiotensin II-induced renal injury and fibrosis in a mouse model #MMPMID30030497 Yu X; Xia Y; Zeng L; Zhang X; Chen L; Yan S; Zhang R; Zhao C; Zeng Z; Shu Y; Huang S; Lei J; Yuan C; Zhang L; Feng Y; Liu W; Huang B; Zhang B; Luo W; Wang X; Zhang H; Haydon RC; Luu HH; He TC; Gan H Sci Rep 2018[]; 8 (ä): ä PMID30030497show ga Chronic kidney disease (CKD) poses a formidable challenge for public healthcare worldwide as vast majority of patients with CKD are also at risk of accelerated cardiovascular disease and death. Renal fibrosis is the common manifestation of CKD that usually leads to end-stage renal disease although the molecular events leading to chronic renal fibrosis and eventually chronic renal failure remain to be fully understood. Nonetheless, emerging evidence suggests that an aberrant activation of PI3K? signaling may play an important role in regulating profibrotic phenotypes. Here, we investigate whether a blockade of PI3K? signaling exerts any beneficial effect on alleviating kidney injury and renal fibrosis. Using a mouse model of angiotensin II (Ang II)-induced renal damage, we demonstrate that PI3K? inhibitor AS605240 effectively mitigates Ang II-induced increases in serum creatinine and blood urea nitrogen, renal interstitial collagen deposition, the accumulation of ECM proteins and the expression of ?-Sma and fibrosis-related genes in vivo. Mechanistically, we reveal that AS605240 effectively inhibits Ang II-induced cell proliferation and phosphorylation of Akt in fibroblast cells. Furthermore, we demonstrate that Ang II-upregulated expression of IL-6, Tnf-?, IL-1? and Tgf-?1 is significantly attenuated in the mice treated with AS605240. Taken together, our results demonstrate that PI3K? may function as a critical mediator of Ang II-induced renal injury and fibrosis. It is thus conceivable that targeted inhibition of PI3K? signaling may constitute a novel therapeutic approach to the clinical management of renal fibrosis, renal hypertension and/or CKD. äA blockade of PI3K? signaling effectively mitigates angiotensin II-ind(epmc).pdf DeepDyve Pubget Overpricing