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10.1016/j.mce.2016.03.038 http://scihub22266oqcxt.onion/10.1016/j.mce.2016.03.038 C4861697!4861697!27040306     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27040306&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27040306.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Cell+Endocrinol 2016 ; 429 (ä): 84-92 Nephropedia Template TP {{tp|p=27040306|t=2016. TRAF3IP2 Mediates Aldosterone/Salt-Induced Cardiac Hypertrophy and Fibrosis |pdf=|usr=}}{{27040306}} gab.com Text TRAF3IP2 Mediates Aldosterone/Salt-Induced Cardiac Hypertrophy and Fibrosis JO: Mol Cell Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=27040306 #FOAvip Aberrant activation of the renin-angiotensin-aldosterone system (RAAS) contributes to adverse cardiac remodeling and eventual failure. Here we investigated whether TRAF3-interacting Protein 2 (TRAF3IP2), a redox-sensitive cytoplasmic adaptor molecule and an upstream regulator of nuclear factor-?B (NF-?B) and activator protein-1 (AP-1), mediates aldosterone-induced cardiac hypertrophy and fibrosis. Wild type (WT) and TRAF3IP2-null mice were infused with aldosterone (0.2mg/kg/day) for 4 weeks along with 1%NaCl in drinking water. Aldosterone/salt, but not salt alone, upregulated TRAF3IP2 expression in WT mouse hearts. Aldosterone elevated blood pressure to a similar extent in both WT and TRAF3IP2-null groups. Importantly, TRAF3IP2 gene deletion attenuated aldosterone/salt-induced (i) p65 and c-Jun activation, (ii) extracellular matrix (collagen I?1 and collagen 3?1), matrix metalloproteinase (MMP2), lysyl oxidase (LOX), inflammatory cytokine (IL-6 and IL-18), chemokine (CXCL1 and CXCL2), and adhesion molecule (ICAM1) gene expression in hearts, (iii) IL-6, IL-18, and MMP2 protein levels, (iv) systemic IL-6 and IL-18 levels, and (iv) cardiac hypertrophy and fibrosis. These results indicate that TRAF3IP2 is a critical signaling intermediate in aldosterone/salt-induced myocardial hypertrophy and fibrosis, and thus a potential therapeutic target in hypertensive heart disease. Twit Text FOAVip TRAF3IP2 Mediates Aldosterone/Salt-Induced Cardiac Hypertrophy and Fibrosis ????Mol Cell Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=27040306 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27040306 #FOAvip English Wikipedia <ref>{{Cite pmid|27040306}}</ref> TRAF3IP2 Mediates Aldosterone/Salt-Induced Cardiac Hypertrophy and Fibrosis #MMPMID27040306 Sakamuri SS; Valente AJ; Siddesha JM; Delafontaine P; Siebenlist U; Gardner JD; Chandrasekar B Mol Cell Endocrinol 2016[Jul]; 429 (ä): 84-92 PMID27040306show ga Aberrant activation of the renin-angiotensin-aldosterone system (RAAS) contributes to adverse cardiac remodeling and eventual failure. Here we investigated whether TRAF3-interacting Protein 2 (TRAF3IP2), a redox-sensitive cytoplasmic adaptor molecule and an upstream regulator of nuclear factor-?B (NF-?B) and activator protein-1 (AP-1), mediates aldosterone-induced cardiac hypertrophy and fibrosis. Wild type (WT) and TRAF3IP2-null mice were infused with aldosterone (0.2mg/kg/day) for 4 weeks along with 1%NaCl in drinking water. Aldosterone/salt, but not salt alone, upregulated TRAF3IP2 expression in WT mouse hearts. Aldosterone elevated blood pressure to a similar extent in both WT and TRAF3IP2-null groups. Importantly, TRAF3IP2 gene deletion attenuated aldosterone/salt-induced (i) p65 and c-Jun activation, (ii) extracellular matrix (collagen I?1 and collagen 3?1), matrix metalloproteinase (MMP2), lysyl oxidase (LOX), inflammatory cytokine (IL-6 and IL-18), chemokine (CXCL1 and CXCL2), and adhesion molecule (ICAM1) gene expression in hearts, (iii) IL-6, IL-18, and MMP2 protein levels, (iv) systemic IL-6 and IL-18 levels, and (iv) cardiac hypertrophy and fibrosis. These results indicate that TRAF3IP2 is a critical signaling intermediate in aldosterone/salt-induced myocardial hypertrophy and fibrosis, and thus a potential therapeutic target in hypertensive heart disease. äTRAF3IP2 Mediates Aldosterone/Salt-Induced Cardiac Hypertrophy and Fib(epmc).pdf DeepDyve Pubget Overpricing