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10.1371/journal.pone.0142456 http://scihub22266oqcxt.onion/10.1371/journal.pone.0142456 C4640881!4640881 !26556241     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26556241 &cmd=llinks): Failed to open stream: HTTP request failed! 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TAK-242, a Toll-Like Receptor 4 Antagonist, Protects against Aldosterone-Induced Cardiac and Renal Injury |pdf=|usr=}}{{26556241 }} gab.com Text TAK-242, a Toll-Like Receptor 4 Antagonist, Protects against Aldosterone-Induced Cardiac and Renal Injury JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26556241 #FOAvip Cardiovascular and renal inflammation induced by Aldosterone (Aldo) plays an important role in the pathogenesis of hypertension and renal fibrosis. Toll-like receptor 4 (TLR4) signaling contributes to inflammatory cardiovascular and renal diseases, but its role in Aldo-induced hypertension and renal damage is not clear. In the current study, rats were treated with Aldo-salt combined with TAK-242 (a TLR4 signaling antagonist) for 4 weeks. Hemodynamic, cardiac and renal parameters were assayed at the indicated time. We found that Aldo-salt-treated rats present cardiac and renal hypertrophy and dysfunction. Cardiac and renal expression levels of TLR4 as well as levels of molecular markers attesting inflammation and fibrosis are increased by Aldo infusion, whereas the treatment of TAK-242 reverses these alterations. TAK-242 suppresses cardiac and renal inflammatory cytokines levels (TNF-a, IL-1? and MCP-1). Furthermore, TAK-242 inhibits hypertension, cardiac and renal fibrosis, and also attenuates the Aldo-induced Epithelial-Mesenchymal Transition (EMT). In experimental hyperaldosteronism, upregulation of TLR4 is correlated with cardiac and renal fibrosis and dysfunction, and a TLR4 signaling antagonist, TAK-242, can reverse these alterations. TAK-242 may be a therapeutic option for salt-sensitive hypertension and renal fibrosis. Twit Text FOAVip TAK-242, a Toll-Like Receptor 4 Antagonist, Protects against Aldosterone-Induced Cardiac and Renal Injury ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26556241 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26556241 #FOAvip English Wikipedia <ref>{{Cite pmid|26556241 }}</ref> TAK-242, a Toll-Like Receptor 4 Antagonist, Protects against Aldosterone-Induced Cardiac and Renal Injury #MMPMID26556241 Zhang Y ; Peng W ; Ao X ; Dai H ; Yuan L ; Huang X ; Zhou Q PLoS One 2015[]; 10 (11 ): e0142456 PMID26556241 show ga Cardiovascular and renal inflammation induced by Aldosterone (Aldo) plays an important role in the pathogenesis of hypertension and renal fibrosis. Toll-like receptor 4 (TLR4) signaling contributes to inflammatory cardiovascular and renal diseases, but its role in Aldo-induced hypertension and renal damage is not clear. In the current study, rats were treated with Aldo-salt combined with TAK-242 (a TLR4 signaling antagonist) for 4 weeks. Hemodynamic, cardiac and renal parameters were assayed at the indicated time. We found that Aldo-salt-treated rats present cardiac and renal hypertrophy and dysfunction. Cardiac and renal expression levels of TLR4 as well as levels of molecular markers attesting inflammation and fibrosis are increased by Aldo infusion, whereas the treatment of TAK-242 reverses these alterations. TAK-242 suppresses cardiac and renal inflammatory cytokines levels (TNF-a, IL-1? and MCP-1). Furthermore, TAK-242 inhibits hypertension, cardiac and renal fibrosis, and also attenuates the Aldo-induced Epithelial-Mesenchymal Transition (EMT). In experimental hyperaldosteronism, upregulation of TLR4 is correlated with cardiac and renal fibrosis and dysfunction, and a TLR4 signaling antagonist, TAK-242, can reverse these alterations. TAK-242 may be a therapeutic option for salt-sensitive hypertension and renal fibrosis. |*Aldosterone [MESH] |Acute Kidney Injury/blood/chemically induced/physiopathology/*prevention & control [MESH] |Animals [MESH] |Cytokines/blood [MESH] |Heart Diseases/blood/chemically induced/physiopathology/*prevention & control [MESH] |Hemodynamics/drug effects/physiology [MESH] |Inflammation/blood/chemically induced/physiopathology/prevention & control [MESH] |Male [MESH] |Protective Agents/*pharmacology/therapeutic use [MESH] |Rats [MESH] |Rats, Wistar [MESH] |Sulfonamides/*pharmacology/therapeutic use [MESH]TAK-242, a Toll-Like Receptor 4 Antagonist, Protects against Aldostero(epmc).pdf DeepDyve Pubget Overpricing