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10.1126/science.abe4832 http://scihub22266oqcxt.onion/10.1126/science.abe4832 34103349!8607935!34103349     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34103349&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 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34103349.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Science 2021 ; 373 (6552): � Nephropedia Template TP {{tp|p=34103349|t=2021. Senolytics reduce coronavirus-related mortality in old mice |pdf=|usr=}}{{34103349}} gab.com Text Senolytics reduce coronavirus-related mortality in old mice JO: Science http://www.kidney.de/pget.php?&tw=1&pmid=34103349 #FOAvip The COVID-19 pandemic has revealed the pronounced vulnerability of the elderly and chronically ill to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced morbidity and mortality. Cellular senescence contributes to inflammation, multiple chronic diseases, and age-related dysfunction, but effects on responses to viral infection are unclear. Here, we demonstrate that senescent cells (SnCs) become hyper-inflammatory in response to pathogen-associated molecular patterns (PAMPs), including SARS-CoV-2 spike protein-1, increasing expression of viral entry proteins and reducing antiviral gene expression in non-SnCs through a paracrine mechanism. Old mice acutely infected with pathogens that included a SARS-CoV-2-related mouse beta-coronavirus experienced increased senescence and inflammation, with nearly 100% mortality. Targeting SnCs by using senolytic drugs before or after pathogen exposure significantly reduced mortality, cellular senescence, and inflammatory markers and increased antiviral antibodies. Thus, reducing the SnC burden in diseased or aged individuals should enhance resilience and reduce mortality after viral infection, including that of SARS-CoV-2. Twit Text FOAVip Senolytics reduce coronavirus-related mortality in old mice ????Science http://www.kidney.de/pget.php?&tw=1&pmid=34103349 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34103349 #FOAvip English Wikipedia <ref>{{Cite pmid|34103349}}</ref> Senolytics reduce coronavirus-related mortality in old mice #MMPMID34103349 Camell CD; Yousefzadeh MJ; Zhu Y; Prata LGPL; Huggins MA; Pierson M; Zhang L; O'Kelly RD; Pirtskhalava T; Xun P; Ejima K; Xue A; Tripathi U; Espindola-Netto JM; Giorgadze N; Atkinson EJ; Inman CL; Johnson KO; Cholensky SH; Carlson TW; LeBrasseur NK; Khosla S; O'Sullivan MG; Allison DB; Jameson SC; Meves A; Li M; Prakash YS; Chiarella SE; Hamilton SE; Tchkonia T; Niedernhofer LJ; Kirkland JL; Robbins PD Science 2021[Jul]; 373 (6552): � PMID34103349show ga The COVID-19 pandemic has revealed the pronounced vulnerability of the elderly and chronically ill to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced morbidity and mortality. Cellular senescence contributes to inflammation, multiple chronic diseases, and age-related dysfunction, but effects on responses to viral infection are unclear. Here, we demonstrate that senescent cells (SnCs) become hyper-inflammatory in response to pathogen-associated molecular patterns (PAMPs), including SARS-CoV-2 spike protein-1, increasing expression of viral entry proteins and reducing antiviral gene expression in non-SnCs through a paracrine mechanism. Old mice acutely infected with pathogens that included a SARS-CoV-2-related mouse beta-coronavirus experienced increased senescence and inflammation, with nearly 100% mortality. Targeting SnCs by using senolytic drugs before or after pathogen exposure significantly reduced mortality, cellular senescence, and inflammatory markers and increased antiviral antibodies. Thus, reducing the SnC burden in diseased or aged individuals should enhance resilience and reduce mortality after viral infection, including that of SARS-CoV-2. |*Aging[MESH] |Animals[MESH] |COVID-19 Drug Treatment[MESH] |COVID-19/immunology/mortality[MESH] |Cell Line[MESH] |Cellular Senescence/*drug effects[MESH] |Coronavirus Infections/immunology/*mortality[MESH] |Dasatinib/pharmacology/therapeutic use[MESH] |Female[MESH] |Flavonols/pharmacology/*therapeutic use[MESH] |Gene Expression Regulation[MESH] |Humans[MESH] |Lipopolysaccharides[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Murine hepatitis virus/immunology[MESH] |Pathogen-Associated Molecular Pattern Molecules/*metabolism[MESH] |Quercetin/pharmacology/therapeutic use[MESH] |Receptors, Coronavirus/genetics/metabolism[MESH] |Specific Pathogen-Free Organisms[MESH]Senolytics reduce coronavirus-related mortality in old mice (epmc).pdf DeepDyve Pubget Overpricing