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10.1038/s41418-020-00690-y http://scihub22266oqcxt.onion/10.1038/s41418-020-00690-y 33273695!7712602!33273695     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Differ 2021 ; 28 (5): 1610-1626 Nephropedia Template TP {{tp|p=33273695|t=2021. Primidone blocks RIPK1-driven cell death and inflammation |pdf=|usr=}}{{33273695}} gab.com Text Primidone blocks RIPK1-driven cell death and inflammation JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=33273695 #FOAvip The receptor-interacting serine/threonine protein kinase 1 (RIPK1) is a key mediator of regulated cell death and inflammation. Recent studies suggest that RIPK1 inhibition would fundamentally improve the therapy of RIPK1-dependent organ damage in stroke, myocardial infarction, kidney failure, and systemic inflammatory response syndrome. Additionally, it could ameliorate or prevent multi-organ failure induced by cytokine release in the context of hyperinflammation, as seen in COVID-19 patients. Therefore, we searched for a RIPK1 inhibitor and present the aromatic antiepileptic and FDA-approved drug primidone (Liskantin(R)) as a potent inhibitor of RIPK1 activation in vitro and in a murine model of TNFalpha-induced shock, which mimics the hyperinflammatory state of cytokine release syndrome. Furthermore, we detected for the first time RIPK1 activation in the respiratory tract epithelium of hospitalized patients who tested positive for SARS-CoV-2 infection. Our data provide a strong rationale for evaluating the drug primidone in conditions of hyperinflammation in humans. Twit Text FOAVip Primidone blocks RIPK1-driven cell death and inflammation ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=33273695 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33273695 #FOAvip English Wikipedia <ref>{{Cite pmid|33273695}}</ref> Primidone blocks RIPK1-driven cell death and inflammation #MMPMID33273695 Riebeling T; Jamal K; Wilson R; Kolbrink B; von Samson-Himmelstjerna FA; Moerke C; Ramos Garcia L; Dahlke E; Michels F; Luhder F; Schunk D; Doldi P; Tyczynski B; Kribben A; Fluh C; Theilig F; Kunzendorf U; Meier P; Krautwald S Cell Death Differ 2021[May]; 28 (5): 1610-1626 PMID33273695show ga The receptor-interacting serine/threonine protein kinase 1 (RIPK1) is a key mediator of regulated cell death and inflammation. Recent studies suggest that RIPK1 inhibition would fundamentally improve the therapy of RIPK1-dependent organ damage in stroke, myocardial infarction, kidney failure, and systemic inflammatory response syndrome. Additionally, it could ameliorate or prevent multi-organ failure induced by cytokine release in the context of hyperinflammation, as seen in COVID-19 patients. Therefore, we searched for a RIPK1 inhibitor and present the aromatic antiepileptic and FDA-approved drug primidone (Liskantin(R)) as a potent inhibitor of RIPK1 activation in vitro and in a murine model of TNFalpha-induced shock, which mimics the hyperinflammatory state of cytokine release syndrome. Furthermore, we detected for the first time RIPK1 activation in the respiratory tract epithelium of hospitalized patients who tested positive for SARS-CoV-2 infection. Our data provide a strong rationale for evaluating the drug primidone in conditions of hyperinflammation in humans. |Animals[MESH] |COVID-19 Drug Treatment[MESH] |COVID-19/*enzymology/pathology[MESH] |Cell Death/drug effects[MESH] |HEK293 Cells[MESH] |HT29 Cells[MESH] |Humans[MESH] |Inflammation/drug therapy/enzymology/pathology[MESH] |Jurkat Cells[MESH] |Mice[MESH] |NIH 3T3 Cells[MESH] |Primidone/*pharmacology[MESH] |Receptor-Interacting Protein Serine-Threonine Kinases/*metabolism[MESH] |SARS-CoV-2/*metabolism[MESH]Primidone blocks RIPK1-driven cell death and inflammation (epmc).pdf DeepDyve Pubget Overpricing