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10.1038/s41419-017-0123-3 http://scihub22266oqcxt.onion/10.1038/s41419-017-0123-3 C5833382!5833382!29367637     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 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2018 ; 9 (2): ä Nephropedia Template TP {{tp|p=29367637|t=2018. Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPK?/Smad3 signaling |pdf=|usr=}}{{29367637}} gab.com Text Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPK /Smad3 signaling JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29367637 #FOAvip Agonists of peroxisome proliferator-activated receptor gamma (PPAR-?) can activate 5? AMP-activated protein kinase alpha (AMPK?) and exert cardioprotective effects. A previous study has demonstrated that rosmarinic acid (RA) can activate PPAR-?, but its effect on cardiac remodeling remains largely unknown. Our study aimed to investigate the effect of RA on cardiac remodeling and to clarify the underlying mechanism. Mice were subjected to aortic banding to generate pressure overload induced cardiac remodeling and then were orally administered RA (100?mg/kg/day) for 7 weeks beginning 1 week after surgery. The morphological examination, echocardiography, and molecular markers were used to evaluate the effects of RA. To ascertain whether the beneficial effect of RA on cardiac fibrosis was mediated by AMPK?, AMPK?2 knockout mice were used. Neonatal rat cardiomyocytes and fibroblasts were separated and cultured to validate the protective effect of RA in vitro. RA-treated mice exhibited a similar hypertrophic response as mice without RA treatment, but had an attenuated fibrotic response and improved cardiac function after pressure overload. Activated AMPK? was essential for the anti-fibrotic effect of RA via inhibiting the phosphorylation and nuclear translocation of Smad3 in vivo and in vitro, and AMPK? deficiency abolished RA-mediated protective effects. Small interfering RNA against Ppar-? (siPpar-?) and GW9662, a specific antagonist of PPAR-?, abolished RA-mediated AMPK? phosphorylation and alleviation of fibrotic response in vitro. RA attenuated cardiac fibrosis following long-term pressure overload via AMPK?/Smad3 signaling and PPAR-? was required for the activation of AMPK?. RA might be a promising therapeutic agent against cardiac fibrosis. Twit Text FOAVip Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPK /Smad3 signaling ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29367637 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29367637 #FOAvip English Wikipedia <ref>{{Cite pmid|29367637}}</ref> Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPK?/Smad3 signaling #MMPMID29367637 Zhang X; Ma ZG; Yuan YP; Xu SC; Wei WY; Song P; Kong CY; Deng W; Tang QZ Cell Death Dis 2018[Feb]; 9 (2): ä PMID29367637show ga Agonists of peroxisome proliferator-activated receptor gamma (PPAR-?) can activate 5? AMP-activated protein kinase alpha (AMPK?) and exert cardioprotective effects. A previous study has demonstrated that rosmarinic acid (RA) can activate PPAR-?, but its effect on cardiac remodeling remains largely unknown. Our study aimed to investigate the effect of RA on cardiac remodeling and to clarify the underlying mechanism. Mice were subjected to aortic banding to generate pressure overload induced cardiac remodeling and then were orally administered RA (100?mg/kg/day) for 7 weeks beginning 1 week after surgery. The morphological examination, echocardiography, and molecular markers were used to evaluate the effects of RA. To ascertain whether the beneficial effect of RA on cardiac fibrosis was mediated by AMPK?, AMPK?2 knockout mice were used. Neonatal rat cardiomyocytes and fibroblasts were separated and cultured to validate the protective effect of RA in vitro. RA-treated mice exhibited a similar hypertrophic response as mice without RA treatment, but had an attenuated fibrotic response and improved cardiac function after pressure overload. Activated AMPK? was essential for the anti-fibrotic effect of RA via inhibiting the phosphorylation and nuclear translocation of Smad3 in vivo and in vitro, and AMPK? deficiency abolished RA-mediated protective effects. Small interfering RNA against Ppar-? (siPpar-?) and GW9662, a specific antagonist of PPAR-?, abolished RA-mediated AMPK? phosphorylation and alleviation of fibrotic response in vitro. RA attenuated cardiac fibrosis following long-term pressure overload via AMPK?/Smad3 signaling and PPAR-? was required for the activation of AMPK?. RA might be a promising therapeutic agent against cardiac fibrosis. äRosmarinic acid attenuates cardiac fibrosis following long-term pressu(epmc).pdf DeepDyve Pubget Overpricing