Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

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.

10.1097/MNH.0000000000000205 http://scihub22266oqcxt.onion/10.1097/MNH.0000000000000205 C4770891!4770891!26808707     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Opin+Nephrol+Hypertens 2016 ; 25 (2): 100-6 Nephropedia Template TP {{tp|p=26808707|t=2016. Wnt/?-catenin signaling and renin-angiotensin system in chronic kidney disease |pdf=|usr=}}{{26808707}} gab.com Text Wnt/ -catenin signaling and renin-angiotensin system in chronic kidney disease JO: Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=26808707 #FOAvip Purpose of review: Intrarenal activation of the renin?angiotensin system (RAS) plays an essential role in the pathogenesis of hypertension and chronic kidney diseases (CKD). However, how RAS genes are regulated in vivo was poorly understood until recently. This review focuses on recent findings of the transcriptional regulation of RAS components as well as their implication in developing novel strategies to treat the patients with CKD. Recent findings: Bioinformatics analyses have uncovered the presence of putative binding sites for T cell factor (TCF)/?-catenin in the promoter region of all RAS genes. Both in vitro and in vivo studies confirm that Wnt/?-catenin is the master upstream regulator that controls the expression of all RAS components tested such as angiotensinogen, renin, angiotensin converting enzyme (ACE) and angiotensin II type I receptor (AT1) in the kidney. Targeted inhibition of Wnt/?-catenin, by either small molecule ICG-001 or endogenous Wnt antagonist Klotho, represses RAS activation and ameliorates proteinuria and kidney injury. Blockade of Wnt/?-catenin signaling also normalizes blood pressure in mouse model of CKD. Summary: These recent studies identify Wnt/?-catenin as the master regulator that controls multiple RAS genes, and suggest that targeting this upstream signaling could be an effective strategy for the treatment of patients with hypertension and CKD. Twit Text FOAVip Wnt/ -catenin signaling and renin-angiotensin system in chronic kidney disease ????Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=26808707 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26808707 #FOAvip English Wikipedia <ref>{{Cite pmid|26808707}}</ref> Wnt/?-catenin signaling and renin-angiotensin system in chronic kidney disease #MMPMID26808707 Zhou L; Liu Y Curr Opin Nephrol Hypertens 2016[Mar]; 25 (2): 100-6 PMID26808707show ga Purpose of review: Intrarenal activation of the renin?angiotensin system (RAS) plays an essential role in the pathogenesis of hypertension and chronic kidney diseases (CKD). However, how RAS genes are regulated in vivo was poorly understood until recently. This review focuses on recent findings of the transcriptional regulation of RAS components as well as their implication in developing novel strategies to treat the patients with CKD. Recent findings: Bioinformatics analyses have uncovered the presence of putative binding sites for T cell factor (TCF)/?-catenin in the promoter region of all RAS genes. Both in vitro and in vivo studies confirm that Wnt/?-catenin is the master upstream regulator that controls the expression of all RAS components tested such as angiotensinogen, renin, angiotensin converting enzyme (ACE) and angiotensin II type I receptor (AT1) in the kidney. Targeted inhibition of Wnt/?-catenin, by either small molecule ICG-001 or endogenous Wnt antagonist Klotho, represses RAS activation and ameliorates proteinuria and kidney injury. Blockade of Wnt/?-catenin signaling also normalizes blood pressure in mouse model of CKD. Summary: These recent studies identify Wnt/?-catenin as the master regulator that controls multiple RAS genes, and suggest that targeting this upstream signaling could be an effective strategy for the treatment of patients with hypertension and CKD. äWnt/?-catenin signaling and renin-angiotensin system in chronic kidney(epmc).pdf DeepDyve Pubget Overpricing