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10.1161/CIRCULATIONAHA.115.018174 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.115.018174 C5446084!5446084!26585673     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circulation 2016 ; 133 (3): 291-301 Nephropedia Template TP {{tp|p=26585673|t=2016. MiR-125b is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis |pdf=|usr=}}{{26585673}} gab.com Text MiR-125b is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=26585673 #FOAvip Background: Cardiac fibrosis is the pathological consequence of stress-induced fibroblast proliferation and fibroblast-to-myofibroblast transition (FMT). MicroRNAs have been shown to play a central role in the pathogenesis of cardiac fibrosis. We identified a novel miRNA-driven mechanism that promotes cardiac fibrosis via regulation of multiple fibrogenic pathways. Methods and Results: Using a combination of in vitro and in vivo studies, we identified that miR-125b is a novel regulator of cardiac fibrosis, proliferation and activation of cardiac fibroblasts. We demonstrate that miR-125b is induced in both fibrotic human heart and murine models of cardiac fibrosis. In addition, our results indicate that miR-125b is necessary and sufficient for the induction of FMT by functionally targeting apelin, a critical repressor of fibrogenesis. Furthermore, we observed that miR-125b inhibits p53 to induce fibroblast proliferation. Most importantly, in vivo silencing of miR-125b by systemic delivery of locked nucleic acid (LNA) rescued Angiotensin II-induced perivascular and interstitial fibrosis. Finally, the RNA-sequencing analysis established that miR-125b altered the gene expression profiles of the key fibrosis-related genes and is a core component of fibrogenesis in the heart. Conclusions: In conclusion, miR-125b is critical for induction of cardiac fibrosis and acts as a potent repressor of multiple anti-fibrotic mechanisms. Inhibition of miR-125b may represent a novel therapeutic approach for the treatment of human cardiac fibrosis and other fibrotic diseases. Twit Text FOAVip MiR-125b is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=26585673 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26585673 #FOAvip English Wikipedia <ref>{{Cite pmid|26585673}}</ref> MiR-125b is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis #MMPMID26585673 Nagpal V; Rai R; Place AT; Murphy SB; Verma SK; Ghosh AK; Vaughan DE Circulation 2016[Jan]; 133 (3): 291-301 PMID26585673show ga Background: Cardiac fibrosis is the pathological consequence of stress-induced fibroblast proliferation and fibroblast-to-myofibroblast transition (FMT). MicroRNAs have been shown to play a central role in the pathogenesis of cardiac fibrosis. We identified a novel miRNA-driven mechanism that promotes cardiac fibrosis via regulation of multiple fibrogenic pathways. Methods and Results: Using a combination of in vitro and in vivo studies, we identified that miR-125b is a novel regulator of cardiac fibrosis, proliferation and activation of cardiac fibroblasts. We demonstrate that miR-125b is induced in both fibrotic human heart and murine models of cardiac fibrosis. In addition, our results indicate that miR-125b is necessary and sufficient for the induction of FMT by functionally targeting apelin, a critical repressor of fibrogenesis. Furthermore, we observed that miR-125b inhibits p53 to induce fibroblast proliferation. Most importantly, in vivo silencing of miR-125b by systemic delivery of locked nucleic acid (LNA) rescued Angiotensin II-induced perivascular and interstitial fibrosis. Finally, the RNA-sequencing analysis established that miR-125b altered the gene expression profiles of the key fibrosis-related genes and is a core component of fibrogenesis in the heart. Conclusions: In conclusion, miR-125b is critical for induction of cardiac fibrosis and acts as a potent repressor of multiple anti-fibrotic mechanisms. Inhibition of miR-125b may represent a novel therapeutic approach for the treatment of human cardiac fibrosis and other fibrotic diseases. äMiR-125b is Critical for Fibroblast-to-Myofibroblast Transition and Ca(epmc).pdf DeepDyve Pubget Overpricing