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10.1016/j.mito.2020.06.008 http://scihub22266oqcxt.onion/10.1016/j.mito.2020.06.008 32574708!7837003!32574708     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       Mitochondrion 2020 ; 54 (ä): 1-7 Nephropedia Template TP {{tp|p=32574708|t=2020. Mitochondria and microbiota dysfunction in COVID-19 pathogenesis |pdf=|usr=}}{{32574708}} gab.com Text Mitochondria and microbiota dysfunction in COVID-19 pathogenesis JO: Mitochondrion http://www.kidney.de/pget.php?&tw=1&pmid=32574708 #FOAvip The COVID-19 pandemic caused by the coronavirus (SARS-CoV-2) has taken the world by surprise into a major crisis of overwhelming morbidity and mortality. This highly infectious disease is associated with respiratory failure unusual in other coronavirus infections. Mounting evidence link the accelerated progression of the disease in COVID-19 patients to the hyper-inflammatory state termed as the "cytokine storm" involving major systemic perturbations. These include iron dysregulation manifested as hyperferritinemia associated with disease severity. Iron dysregulation induces reactive oxygen species (ROS) production and promotes oxidative stress. The mitochondria are the hub of cellular oxidative homeostasis. In addition, the mitochondria may circulate "cell-free" in non-nucleated platelets, in extracellular vesicles and mitochondrial DNA is found in the extracellular space. The heightened inflammatory/oxidative state may lead to mitochondrial dysfunction leading to platelet damage and apoptosis. The interaction of dysfunctional platelets with coagulation cascades aggravates clotting events and thrombus formation. Furthermore, mitochondrial oxidative stress may contribute to microbiota dysbiosis, altering coagulation pathways and fueling the inflammatory/oxidative response leading to the vicious cycle of events. Here, we discuss various cellular and systemic incidents caused by SARS-CoV-2 that may critically impact intra and extracellular mitochondrial function, and contribute to the progression and severity of the disease. It is crucial to understand how these key modulators impact COVID-19 pathogenesis in the quest to identify novel therapeutic targets that may reduce fatal outcomes of the disease. Twit Text FOAVip Mitochondria and microbiota dysfunction in COVID-19 pathogenesis ????Mitochondrion http://www.kidney.de/pget.php?&tw=1&pmid=32574708 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32574708 #FOAvip English Wikipedia <ref>{{Cite pmid|32574708}}</ref> Mitochondria and microbiota dysfunction in COVID-19 pathogenesis #MMPMID32574708 Saleh J; Peyssonnaux C; Singh KK; Edeas M Mitochondrion 2020[Sep]; 54 (ä): 1-7 PMID32574708show ga The COVID-19 pandemic caused by the coronavirus (SARS-CoV-2) has taken the world by surprise into a major crisis of overwhelming morbidity and mortality. This highly infectious disease is associated with respiratory failure unusual in other coronavirus infections. Mounting evidence link the accelerated progression of the disease in COVID-19 patients to the hyper-inflammatory state termed as the "cytokine storm" involving major systemic perturbations. These include iron dysregulation manifested as hyperferritinemia associated with disease severity. Iron dysregulation induces reactive oxygen species (ROS) production and promotes oxidative stress. The mitochondria are the hub of cellular oxidative homeostasis. In addition, the mitochondria may circulate "cell-free" in non-nucleated platelets, in extracellular vesicles and mitochondrial DNA is found in the extracellular space. The heightened inflammatory/oxidative state may lead to mitochondrial dysfunction leading to platelet damage and apoptosis. The interaction of dysfunctional platelets with coagulation cascades aggravates clotting events and thrombus formation. Furthermore, mitochondrial oxidative stress may contribute to microbiota dysbiosis, altering coagulation pathways and fueling the inflammatory/oxidative response leading to the vicious cycle of events. Here, we discuss various cellular and systemic incidents caused by SARS-CoV-2 that may critically impact intra and extracellular mitochondrial function, and contribute to the progression and severity of the disease. It is crucial to understand how these key modulators impact COVID-19 pathogenesis in the quest to identify novel therapeutic targets that may reduce fatal outcomes of the disease. |*Betacoronavirus[MESH] |Blood Coagulation Disorders/etiology[MESH] |Blood Platelets[MESH] |COVID-19[MESH] |Cardiolipins/metabolism[MESH] |Coronavirus Infections/*complications[MESH] |Dysbiosis/pathology[MESH] |Homeostasis[MESH] |Humans[MESH] |Inflammation/metabolism[MESH] |Iron[MESH] |Mitochondria/*metabolism[MESH] |Mitochondrial Diseases/*virology[MESH] |Oxidative Stress[MESH] |Pandemics[MESH] |Pneumonia, Viral/*complications[MESH] |SARS-CoV-2[MESH]Mitochondria and microbiota dysfunction in COVID-19 pathogenesis (epmc).pdf DeepDyve Pubget Overpricing