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10.1007/s10545-015-9861-5 http://scihub22266oqcxt.onion/10.1007/s10545-015-9861-5 C4493798!4493798!26025548     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Inherit+Metab+Dis 2015 ; 38 (4): 703-19 Nephropedia Template TP {{tp|p=26025548|t=2015. Redox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism |pdf=|usr=}}{{26025548}} gab.com Text Redox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism JO: J Inherit Metab Dis http://www.kidney.de/pget.php?&tw=1&pmid=26025548 #FOAvip Mitochondria play a key role in overall cell physiology and health by integrating cellular metabolism with cellular defense and repair mechanisms in response to physiological or environmental changes or stresses. In fact, dysregulation of mitochondrial stress responses and its consequences in the form of oxidative stress, has been linked to a wide variety of diseases including inborn errors of metabolism. In this review we will summarize how the functional state of mitochondria ? and especially the concentration of reactive oxygen species (ROS), produced in connection with the respiratory chain ? regulates cellular stress responses by redox regulation of nuclear gene networks involved in repair systems to maintain cellular homeostasis and health. Based on our own and other?s studies we re-introduce the ROS triangle model and discuss how inborn errors of mitochondrial metabolism, by production of pathological amounts of ROS, may cause disturbed redox signalling and induce chronic cell stress with non-resolving or compromised cell repair responses and increased susceptibility to cell stress induced cell death. We suggest that this model may have important implications for those inborn errors of metabolism, where mitochondrial dysfunction plays a major role, as it allows the explanation of oxidative stress, metabolic reprogramming and altered signalling growth pathways that have been reported in many of the diseases. It is our hope that the model may facilitate novel ideas and directions that can be tested experimentally and used in the design of future new approaches for pre-symptomatic diagnosis and prognosis and perhaps more effective treatments of inborn errors of metabolism. Twit Text FOAVip Redox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism ????J Inherit Metab Dis http://www.kidney.de/pget.php?&tw=1&pmid=26025548 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26025548 #FOAvip English Wikipedia <ref>{{Cite pmid|26025548}}</ref> Redox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism #MMPMID26025548 Olsen RKJ; Cornelius N; Gregersen N J Inherit Metab Dis 2015[]; 38 (4): 703-19 PMID26025548show ga Mitochondria play a key role in overall cell physiology and health by integrating cellular metabolism with cellular defense and repair mechanisms in response to physiological or environmental changes or stresses. In fact, dysregulation of mitochondrial stress responses and its consequences in the form of oxidative stress, has been linked to a wide variety of diseases including inborn errors of metabolism. In this review we will summarize how the functional state of mitochondria ? and especially the concentration of reactive oxygen species (ROS), produced in connection with the respiratory chain ? regulates cellular stress responses by redox regulation of nuclear gene networks involved in repair systems to maintain cellular homeostasis and health. Based on our own and other?s studies we re-introduce the ROS triangle model and discuss how inborn errors of mitochondrial metabolism, by production of pathological amounts of ROS, may cause disturbed redox signalling and induce chronic cell stress with non-resolving or compromised cell repair responses and increased susceptibility to cell stress induced cell death. We suggest that this model may have important implications for those inborn errors of metabolism, where mitochondrial dysfunction plays a major role, as it allows the explanation of oxidative stress, metabolic reprogramming and altered signalling growth pathways that have been reported in many of the diseases. It is our hope that the model may facilitate novel ideas and directions that can be tested experimentally and used in the design of future new approaches for pre-symptomatic diagnosis and prognosis and perhaps more effective treatments of inborn errors of metabolism. äRedox signalling and mitochondrial stress responses; lessons from inbo(epmc).pdf DeepDyve Pubget Overpricing