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10.15252/emmm.201404318 http://scihub22266oqcxt.onion/10.15252/emmm.201404318 C4459819!4459819!25828351     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25828351&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2015 ; 7 (6): 802-18 Nephropedia Template TP {{tp|p=25828351|t=2015. Defects in mitophagy promote redox-driven metabolic syndrome in the absence of TP53INP1 |pdf=|usr=}}{{25828351}} gab.com Text Defects in mitophagy promote redox-driven metabolic syndrome in the absence of TP53INP1 JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25828351 #FOAvip The metabolic syndrome covers metabolic abnormalities including obesity and type 2 diabetes (T2D). T2D is characterized by insulin resistance resulting from both environmental and genetic factors. A genome-wide association study (GWAS) published in 2010 identified TP53INP1 as a new T2D susceptibility locus, but a pathological mechanism was not identified. In this work, we show that mice lacking TP53INP1 are prone to redox-driven obesity and insulin resistance. Furthermore, we demonstrate that the reactive oxygen species increase in TP53INP1-deficient cells results from accumulation of defective mitochondria associated with impaired PINK/PARKIN mitophagy. This chronic oxidative stress also favors accumulation of lipid droplets. Taken together, our data provide evidence that the GWAS-identified TP53INP1 gene prevents metabolic syndrome, through a mechanism involving prevention of oxidative stress by mitochondrial homeostasis regulation. In conclusion, this study highlights TP53INP1 as a molecular regulator of redox-driven metabolic syndrome and provides a new preclinical mouse model for metabolic syndrome clinical research. Twit Text FOAVip Defects in mitophagy promote redox-driven metabolic syndrome in the absence of TP53INP1 ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25828351 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25828351 #FOAvip English Wikipedia <ref>{{Cite pmid|25828351}}</ref> Defects in mitophagy promote redox-driven metabolic syndrome in the absence of TP53INP1 #MMPMID25828351 Seillier M; Pouyet L; N'Guessan P; Nollet M; Capo F; Guillaumond F; Peyta L; Dumas JF; Varrault A; Bertrand G; Bonnafous S; Tran A; Meur G; Marchetti P; Ravier MA; Dalle S; Gual P; Muller D; Rutter GA; Servais S; Iovanna JL; Carrier A EMBO Mol Med 2015[Jun]; 7 (6): 802-18 PMID25828351show ga The metabolic syndrome covers metabolic abnormalities including obesity and type 2 diabetes (T2D). T2D is characterized by insulin resistance resulting from both environmental and genetic factors. A genome-wide association study (GWAS) published in 2010 identified TP53INP1 as a new T2D susceptibility locus, but a pathological mechanism was not identified. In this work, we show that mice lacking TP53INP1 are prone to redox-driven obesity and insulin resistance. Furthermore, we demonstrate that the reactive oxygen species increase in TP53INP1-deficient cells results from accumulation of defective mitochondria associated with impaired PINK/PARKIN mitophagy. This chronic oxidative stress also favors accumulation of lipid droplets. Taken together, our data provide evidence that the GWAS-identified TP53INP1 gene prevents metabolic syndrome, through a mechanism involving prevention of oxidative stress by mitochondrial homeostasis regulation. In conclusion, this study highlights TP53INP1 as a molecular regulator of redox-driven metabolic syndrome and provides a new preclinical mouse model for metabolic syndrome clinical research. äDefects in mitophagy promote redox-driven metabolic syndrome in the ab(epmc).pdf DeepDyve Pubget Overpricing