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10.1016/j.isci.2021.103722 http://scihub22266oqcxt.onion/10.1016/j.isci.2021.103722 35005527!8720045!35005527     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       iScience 2022 ; 25 (1): 103722 Nephropedia Template TP {{tp|p=35005527|t=2022. SARS-CoV-2 infection enhances mitochondrial PTP complex activity to perturb cardiac energetics |pdf=|usr=}}{{35005527}} gab.com Text SARS-CoV-2 infection enhances mitochondrial PTP complex activity to perturb cardiac energetics JO: iScience http://www.kidney.de/pget.php?&tw=1&pmid=35005527 #FOAvip SARS-CoV-2 is a newly identified coronavirus that causes the respiratory disease called coronavirus disease 2019 (COVID-19). With an urgent need for therapeutics, we lack a full understanding of the molecular basis of SARS-CoV-2-induced cellular damage and disease progression. Here, we conducted transcriptomic analysis of human PBMCs, identified significant changes in mitochondrial, ion channel, and protein quality-control gene products. SARS-CoV-2 proteins selectively target cellular organelle compartments, including the endoplasmic reticulum and mitochondria. M-protein, NSP6, ORF3A, ORF9C, and ORF10 bind to mitochondrial PTP complex components cyclophilin D, SPG-7, ANT, ATP synthase, and a previously undescribed CCDC58 (coiled-coil domain containing protein 58). Knockdown of CCDC58 or mPTP blocker cyclosporin A pretreatment enhances mitochondrial Ca(2+) retention capacity and bioenergetics. SARS-CoV-2 infection exacerbates cardiomyocyte autophagy and promotes cell death that was suppressed by cyclosporin A treatment. Our findings reveal that SARS-CoV-2 viral proteins suppress cardiomyocyte mitochondrial function that disrupts cardiomyocyte Ca(2+) cycling and cell viability. Twit Text FOAVip SARS-CoV-2 infection enhances mitochondrial PTP complex activity to perturb cardiac energetics ????iScience http://www.kidney.de/pget.php?&tw=1&pmid=35005527 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35005527 #FOAvip English Wikipedia <ref>{{Cite pmid|35005527}}</ref> SARS-CoV-2 infection enhances mitochondrial PTP complex activity to perturb cardiac energetics #MMPMID35005527 Ramachandran K; Maity S; Muthukumar AR; Kandala S; Tomar D; Abd El-Aziz TM; Allen C; Sun Y; Venkatesan M; Madaris TR; Chiem K; Truitt R; Vishnu N; Aune G; Anderson A; Martinez-Sobrido L; Yang W; Stockand JD; Singh BB; Srikantan S; Reeves WB; Madesh M iScience 2022[Jan]; 25 (1): 103722 PMID35005527show ga SARS-CoV-2 is a newly identified coronavirus that causes the respiratory disease called coronavirus disease 2019 (COVID-19). With an urgent need for therapeutics, we lack a full understanding of the molecular basis of SARS-CoV-2-induced cellular damage and disease progression. Here, we conducted transcriptomic analysis of human PBMCs, identified significant changes in mitochondrial, ion channel, and protein quality-control gene products. SARS-CoV-2 proteins selectively target cellular organelle compartments, including the endoplasmic reticulum and mitochondria. M-protein, NSP6, ORF3A, ORF9C, and ORF10 bind to mitochondrial PTP complex components cyclophilin D, SPG-7, ANT, ATP synthase, and a previously undescribed CCDC58 (coiled-coil domain containing protein 58). Knockdown of CCDC58 or mPTP blocker cyclosporin A pretreatment enhances mitochondrial Ca(2+) retention capacity and bioenergetics. SARS-CoV-2 infection exacerbates cardiomyocyte autophagy and promotes cell death that was suppressed by cyclosporin A treatment. Our findings reveal that SARS-CoV-2 viral proteins suppress cardiomyocyte mitochondrial function that disrupts cardiomyocyte Ca(2+) cycling and cell viability. äSARS-CoV-2 infection enhances mitochondrial PTP complex activity to pe(epmc).pdf DeepDyve Pubget Overpricing