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10.1111/jcmm.13464 http://scihub22266oqcxt.onion/10.1111/jcmm.13464 C5824385!5824385!29314607     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 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 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       J+Cell+Mol+Med 2018 ; 22 (3): 1816-25 Nephropedia Template TP {{tp|p=29314607|t=2018. H3 relaxin inhibits the collagen synthesis via ROS? and P2X7R?mediated NLRP3 inflammasome activation in cardiac fibroblasts under high glucose |pdf=|usr=}}{{29314607}} gab.com Text H3 relaxin inhibits the collagen synthesis via ROS and P2X7R mediated NLRP3 inflammasome activation in cardiac fibroblasts under high glucose JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29314607 #FOAvip Excessive production of reactive oxygen species (ROS) and P2X7R activation induced by high glucose increases NLRP3 inflammasome activation, which contributes to the pathogenesis of diabetic cardiomyopathy. Although H3 relaxin has been shown to inhibit cardiac fibrosis induced by isoproterenol, the mechanism has not been well studied. Here, we demonstrated that high glucose (HG) induced the collagen synthesis by activation of the NLRP3 inflammasome, leading to caspase?1 activation, interleukin?1? (IL?1?) and IL?18 secretion in neonatal rat cardiac fibroblasts. Moreover, we used a high?glucose model with neonatal rat cardiac fibroblasts and showed that the activation of ROS and P2X7R was augmented and that ROS? and P2X7R?mediated NLRP3 inflammasome activation was critical for the collagen synthesis. Inhibition of ROS and P2X7R decreased NLRP3 inflammasome?mediated collagen synthesis, similar to the effects of H3 relaxin. Furthermore, H3 relaxin reduced the collagen synthesis via ROS? and P2X7R?mediated NLRP3 inflammasome activation in response to HG. These results provide a mechanism by which H3 relaxin alleviates NLRP3 inflammasome?mediated collagen synthesis?through the inhibition of ROS and P2X7R under HG conditions and suggest that H3 relaxin represents a potential drug for alleviating cardiac fibrosis in diabetic cardiomyopathy. Twit Text FOAVip H3 relaxin inhibits the collagen synthesis via ROS and P2X7R mediated NLRP3 inflammasome activation in cardiac fibroblasts under high glucose ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29314607 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29314607 #FOAvip English Wikipedia <ref>{{Cite pmid|29314607}}</ref> H3 relaxin inhibits the collagen synthesis via ROS? and P2X7R?mediated NLRP3 inflammasome activation in cardiac fibroblasts under high glucose #MMPMID29314607 Zhang X; Fu Y; Li H; Shen L; Chang Q; Pan L; Hong S; Yin X J Cell Mol Med 2018[Mar]; 22 (3): 1816-25 PMID29314607show ga Excessive production of reactive oxygen species (ROS) and P2X7R activation induced by high glucose increases NLRP3 inflammasome activation, which contributes to the pathogenesis of diabetic cardiomyopathy. Although H3 relaxin has been shown to inhibit cardiac fibrosis induced by isoproterenol, the mechanism has not been well studied. Here, we demonstrated that high glucose (HG) induced the collagen synthesis by activation of the NLRP3 inflammasome, leading to caspase?1 activation, interleukin?1? (IL?1?) and IL?18 secretion in neonatal rat cardiac fibroblasts. Moreover, we used a high?glucose model with neonatal rat cardiac fibroblasts and showed that the activation of ROS and P2X7R was augmented and that ROS? and P2X7R?mediated NLRP3 inflammasome activation was critical for the collagen synthesis. Inhibition of ROS and P2X7R decreased NLRP3 inflammasome?mediated collagen synthesis, similar to the effects of H3 relaxin. Furthermore, H3 relaxin reduced the collagen synthesis via ROS? and P2X7R?mediated NLRP3 inflammasome activation in response to HG. These results provide a mechanism by which H3 relaxin alleviates NLRP3 inflammasome?mediated collagen synthesis?through the inhibition of ROS and P2X7R under HG conditions and suggest that H3 relaxin represents a potential drug for alleviating cardiac fibrosis in diabetic cardiomyopathy. äH3 relaxin inhibits the collagen synthesis via ROS? and P2X7R?mediated(epmc).pdf DeepDyve Pubget Overpricing