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10.14800/rci.626 http://scihub22266oqcxt.onion/10.14800/rci.626 C4807609!4807609!27019861     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       Receptors+Clin+Investig 2015 ; 2 (2): e626- Nephropedia Template TP {{tp|p=27019861|t=2015. Mutual inhibitory mechanisms between PPAR? and Hif-1?: implication in pulmonary hypertension |pdf=|usr=}}{{27019861}} gab.com Text Mutual inhibitory mechanisms between PPAR and Hif-1 : implication in pulmonary hypertension JO: Receptors Clin Investig http://www.kidney.de/pget.php?&tw=1&pmid=27019861 #FOAvip Transcription factor hypoxia-inducible factor 1? (Hif-1?) is known for its crucial role in promoting the pathogenesis of pulmonary hypertension (PH). Previous studies have indicated the in-depth mechanisms that Hif-1? increases the distal pulmonary arterial (PA) pressure and vascular remodeling by triggering the intracellular calcium homeostasis, especially the store-operated calcium entry (SOCE) process. In our recent research paper published in the Journal of Molecular Medicine, we found that the transcription factor peroxisome proliferator-activated receptor ? (PPAR?) activation could attenuate the PH pathogenesis by suppressing the elevated distal PA pressure and vascular remodeling. Moreover, these effects are likely mediated through the inhibition of SOCE by suppressing Hif-1?. These results provided convincing evidence and novel mechanisms in supporting the protective roles of PPAR? on PH treatment. Then, by using comprehensive loss-of-function and gain-of-function strategies, we further identified the presence of a mutual inhibitory mechanism between PPAR? and Hif-1?. Basically, under chronic hypoxic stress, accumulated Hif-1? leads to abolished expression of PPAR? and progressive imbalance between PPAR? and Hif-1?, which promotes the PH progression; however, targeted PPAR? restoration approach reversely inhibits Hif-1? level and Hif-1? mediated signaling transduction, which subsequently attenuates the elevated pulmonary arterial pressure and vascular remodeling under PH pathogenesis. Twit Text FOAVip Mutual inhibitory mechanisms between PPAR and Hif-1 : implication in pulmonary hypertension ????Receptors Clin Investig http://www.kidney.de/pget.php?&tw=1&pmid=27019861 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27019861 #FOAvip English Wikipedia <ref>{{Cite pmid|27019861}}</ref> Mutual inhibitory mechanisms between PPAR? and Hif-1?: implication in pulmonary hypertension #MMPMID27019861 Yang K; Jiang Q; Wang Z; Li M; Zhang Q; Lu W; Wang J Receptors Clin Investig 2015[]; 2 (2): e626- PMID27019861show ga Transcription factor hypoxia-inducible factor 1? (Hif-1?) is known for its crucial role in promoting the pathogenesis of pulmonary hypertension (PH). Previous studies have indicated the in-depth mechanisms that Hif-1? increases the distal pulmonary arterial (PA) pressure and vascular remodeling by triggering the intracellular calcium homeostasis, especially the store-operated calcium entry (SOCE) process. In our recent research paper published in the Journal of Molecular Medicine, we found that the transcription factor peroxisome proliferator-activated receptor ? (PPAR?) activation could attenuate the PH pathogenesis by suppressing the elevated distal PA pressure and vascular remodeling. Moreover, these effects are likely mediated through the inhibition of SOCE by suppressing Hif-1?. These results provided convincing evidence and novel mechanisms in supporting the protective roles of PPAR? on PH treatment. Then, by using comprehensive loss-of-function and gain-of-function strategies, we further identified the presence of a mutual inhibitory mechanism between PPAR? and Hif-1?. Basically, under chronic hypoxic stress, accumulated Hif-1? leads to abolished expression of PPAR? and progressive imbalance between PPAR? and Hif-1?, which promotes the PH progression; however, targeted PPAR? restoration approach reversely inhibits Hif-1? level and Hif-1? mediated signaling transduction, which subsequently attenuates the elevated pulmonary arterial pressure and vascular remodeling under PH pathogenesis. äMutual inhibitory mechanisms between PPAR? and Hif-1?: implication in (epmc).pdf DeepDyve Pubget Overpricing