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10.1371/journal.pone.0138625 http://scihub22266oqcxt.onion/10.1371/journal.pone.0138625 C4575195!4575195!26382847     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (9): ä Nephropedia Template TP {{tp|p=26382847|t=2015. mTOR Overactivation and Compromised Autophagy in the Pathogenesis of Pulmonary Fibrosis |pdf=|usr=}}{{26382847}} gab.com Text mTOR Overactivation and Compromised Autophagy in the Pathogenesis of Pulmonary Fibrosis JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26382847 #FOAvip The mammalian target of rapamycin (mTOR) signaling pathway in pulmonary fibrosis was investigated in cell and animal models. mTOR overactivation in alveolar epithelial cells (AECs) was achieved in the conditional and inducible Tsc1 knock-down mice SPC-rtTA/TetO-Cre/Tsc1fx/+ (STT). Doxycycline caused Tsc1 knock-down and consequently mTOR activation in AECs for the STT mice. Mice treated with bleomycin exhibited increased mortality and pulmonary fibrosis compared with control mice. In wild-type C57BL/6J mice, pretreatment with rapamycin attenuated the bleomycin-mediated mortality and fibrosis. Rapamycin-mediated mouse survival benefit was inhibited by chloroquine, an autophagy inhibitor. Autophagosomes were decreased in the lungs after bleomycin exposure. Rapamycin induced the production of autophagosomes and diminished p62. We concluded that mTOR overactivation in AECs and compromised autophagy in the lungs are involved in the pathogenesis of pulmonary fibrosis. The suppression of mTOR and enhancement of autophagy may be used for treatment of pulmonary fibrosis. Twit Text FOAVip mTOR Overactivation and Compromised Autophagy in the Pathogenesis of Pulmonary Fibrosis ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26382847 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26382847 #FOAvip English Wikipedia <ref>{{Cite pmid|26382847}}</ref> mTOR Overactivation and Compromised Autophagy in the Pathogenesis of Pulmonary Fibrosis #MMPMID26382847 Gui YS; Wang L; Tian X; Li X; Ma A; Zhou W; Zeng N; Zhang J; Cai B; Zhang H; Chen JY; Xu KF PLoS One 2015[]; 10 (9): ä PMID26382847show ga The mammalian target of rapamycin (mTOR) signaling pathway in pulmonary fibrosis was investigated in cell and animal models. mTOR overactivation in alveolar epithelial cells (AECs) was achieved in the conditional and inducible Tsc1 knock-down mice SPC-rtTA/TetO-Cre/Tsc1fx/+ (STT). Doxycycline caused Tsc1 knock-down and consequently mTOR activation in AECs for the STT mice. Mice treated with bleomycin exhibited increased mortality and pulmonary fibrosis compared with control mice. In wild-type C57BL/6J mice, pretreatment with rapamycin attenuated the bleomycin-mediated mortality and fibrosis. Rapamycin-mediated mouse survival benefit was inhibited by chloroquine, an autophagy inhibitor. Autophagosomes were decreased in the lungs after bleomycin exposure. Rapamycin induced the production of autophagosomes and diminished p62. We concluded that mTOR overactivation in AECs and compromised autophagy in the lungs are involved in the pathogenesis of pulmonary fibrosis. The suppression of mTOR and enhancement of autophagy may be used for treatment of pulmonary fibrosis. ämTOR Overactivation and Compromised Autophagy in the Pathogenesis of P(epmc).pdf DeepDyve Pubget Overpricing