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10.15252/emmm.201708689 http://scihub22266oqcxt.onion/10.15252/emmm.201708689 C5887903!5887903!29531021     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2018 ; 10 (4): ä Nephropedia Template TP {{tp|p=29531021|t=2018. Tranilast directly targets NLRP3 to treat inflammasome?driven diseases |pdf=|usr=}}{{29531021}} gab.com Text Tranilast directly targets NLRP3 to treat inflammasome driven diseases JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29531021 #FOAvip The dysregulation of NLRP3 inflammasome can cause uncontrolled inflammation and drive the development of a wide variety of human diseases, but the medications targeting NLRP3 inflammasome are not available in clinic. Here, we show that tranilast (TR), an old anti?allergic clinical drug, is a direct NLRP3 inhibitor. TR inhibits NLRP3 inflammasome activation in macrophages, but has no effects on AIM2 or NLRC4 inflammasome activation. Mechanismly, TR directly binds to the NACHT domain of NLRP3 and suppresses the assembly of NLRP3 inflammasome by blocking NLRP3 oligomerization. In vivo experiments show that TR has remarkable preventive or therapeutic effects on the mouse models of NLRP3 inflammasome?related human diseases, including gouty arthritis, cryopyrin?associated autoinflammatory syndromes, and type 2 diabetes. Furthermore, TR is active ex vivo for synovial fluid mononuclear cells from patients with gout. Thus, our study identifies the old drug TR as a direct NLRP3 inhibitor and provides a potentially practical pharmacological approach for treating NLRP3?driven diseases. Twit Text FOAVip Tranilast directly targets NLRP3 to treat inflammasome driven diseases ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29531021 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29531021 #FOAvip English Wikipedia <ref>{{Cite pmid|29531021}}</ref> Tranilast directly targets NLRP3 to treat inflammasome?driven diseases #MMPMID29531021 Huang Y; Jiang H; Chen Y; Wang X; Yang Y; Tao J; Deng X; Liang G; Zhang H; Jiang W; Zhou R EMBO Mol Med 2018[Apr]; 10 (4): ä PMID29531021show ga The dysregulation of NLRP3 inflammasome can cause uncontrolled inflammation and drive the development of a wide variety of human diseases, but the medications targeting NLRP3 inflammasome are not available in clinic. Here, we show that tranilast (TR), an old anti?allergic clinical drug, is a direct NLRP3 inhibitor. TR inhibits NLRP3 inflammasome activation in macrophages, but has no effects on AIM2 or NLRC4 inflammasome activation. Mechanismly, TR directly binds to the NACHT domain of NLRP3 and suppresses the assembly of NLRP3 inflammasome by blocking NLRP3 oligomerization. In vivo experiments show that TR has remarkable preventive or therapeutic effects on the mouse models of NLRP3 inflammasome?related human diseases, including gouty arthritis, cryopyrin?associated autoinflammatory syndromes, and type 2 diabetes. Furthermore, TR is active ex vivo for synovial fluid mononuclear cells from patients with gout. Thus, our study identifies the old drug TR as a direct NLRP3 inhibitor and provides a potentially practical pharmacological approach for treating NLRP3?driven diseases. äTranilast directly targets NLRP3 to treat inflammasome?driven diseases(epmc).pdf DeepDyve Pubget Overpricing