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.

10.3892/mmr.2017.7584 http://scihub22266oqcxt.onion/10.3892/mmr.2017.7584 C5865857!5865857!28944921     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Med+Rep 2017 ; 16 (5): 7287-96 Nephropedia Template TP {{tp|p=28944921|t=2017. Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling |pdf=|usr=}}{{28944921}} gab.com Text Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling JO: Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28944921 #FOAvip Cardiac fibrosis triggered by pressure overload represents one of the major challenges in the treatment of cardiovascular diseases. MicroRNA (miRNA/miR)-155, a member of the small RNA family, has previously been demonstrated to be associated with cardiac inflammation. However, the effect of miR-155 on cardiac fibrosis induced by angiotensin II (Ang II), particularly in cardiac fibroblasts, requires further investigation. The present study aimed to investigate the effect of miR-155 in Ang II-induced cardiac fibrosis using animal models and cardiac fibroblasts. Animal models were established in male miR-155?/? and wild-type (WT) C57Bl/6J mice (10?12 weeks old) by Ang II infusion using subcutaneously implanted minipumps. After 8 weeks of Ang II infusion, the results demonstrated that the deletion of miR-155 in mice markedly ameliorated ventricular remodeling compared with WT mice, as demonstrated by restricted inflammatory responses, decreased heart size, improved cardiac function and reduced myocardial fibrosis. In vitro, overexpression of miR-155 in cardiac fibroblasts led to significantly increased fibroblast to myofibroblast transformation. However, this effect was abrogated by miR-155 silencing. In conclusion, the results of the present study indicate that genetic loss of miR-155 in mice ameliorates cardiac fibrotic remodeling following pressure overload. Therefore, inhibiting miR-155 may have potential as an adjunct to reduce cardiac inflammation in the treatment of cardiac fibrosis. Twit Text FOAVip Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling ????Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28944921 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28944921 #FOAvip English Wikipedia <ref>{{Cite pmid|28944921}}</ref> Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling #MMPMID28944921 Wei Y; Yan X; Yan L; Hu F; Ma W; Wang Y; Lu S; Zeng Q; Wang Z Mol Med Rep 2017[Nov]; 16 (5): 7287-96 PMID28944921show ga Cardiac fibrosis triggered by pressure overload represents one of the major challenges in the treatment of cardiovascular diseases. MicroRNA (miRNA/miR)-155, a member of the small RNA family, has previously been demonstrated to be associated with cardiac inflammation. However, the effect of miR-155 on cardiac fibrosis induced by angiotensin II (Ang II), particularly in cardiac fibroblasts, requires further investigation. The present study aimed to investigate the effect of miR-155 in Ang II-induced cardiac fibrosis using animal models and cardiac fibroblasts. Animal models were established in male miR-155?/? and wild-type (WT) C57Bl/6J mice (10?12 weeks old) by Ang II infusion using subcutaneously implanted minipumps. After 8 weeks of Ang II infusion, the results demonstrated that the deletion of miR-155 in mice markedly ameliorated ventricular remodeling compared with WT mice, as demonstrated by restricted inflammatory responses, decreased heart size, improved cardiac function and reduced myocardial fibrosis. In vitro, overexpression of miR-155 in cardiac fibroblasts led to significantly increased fibroblast to myofibroblast transformation. However, this effect was abrogated by miR-155 silencing. In conclusion, the results of the present study indicate that genetic loss of miR-155 in mice ameliorates cardiac fibrotic remodeling following pressure overload. Therefore, inhibiting miR-155 may have potential as an adjunct to reduce cardiac inflammation in the treatment of cardiac fibrosis. äInhibition of microRNA-155 ameliorates cardiac fibrosis in the process(epmc).pdf DeepDyve Pubget Overpricing