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10.1038/s41598-022-15976-z http://scihub22266oqcxt.onion/10.1038/s41598-022-15976-z 35879338!9314328!35879338     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2022 ; 12 (1): 11855 Nephropedia Template TP {{tp|p=35879338|t=2022. Senescent endothelial cells are predisposed to SARS-CoV-2 infection and subsequent endothelial dysfunction |pdf=|usr=}}{{35879338}} gab.com Text Senescent endothelial cells are predisposed to SARS-CoV-2 infection and subsequent endothelial dysfunction JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=35879338 #FOAvip The coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains to spread worldwide. COVID-19 is characterized by the striking high mortality in elderly; however, its mechanistic insights remain unclear. Systemic thrombosis has been highlighted in the pathogenesis of COVID-19, and lung microangiopathy in association with endothelial cells (ECs) injury has been reported by post-mortem analysis of the lungs. Here, we experimentally investigated the SARS-CoV-2 infection in cultured human ECs, and performed a comparative analysis for post-infection molecular events using early passage and replicative senescent ECs. We found that; (1) SARS-CoV-2 infects ECs but does not replicate and disappears in 72 hours without causing severe cell damage, (2) Senescent ECs are highly susceptible to SARS-CoV-2 infection, (3) SARS-CoV-2 infection alters various genes expression, which could cause EC dysfunctions, (4) More genes expression is affected in senescent ECs by SARS-CoV-2 infection than in early passage ECs, which might causes further exacerbated dysfunction in senescent ECs. These data suggest that sustained EC dysfunctions due to SARS-CoV-2 infection may contribute to the microangiopathy in the lungs, leading to deteriorated inflammation and thrombosis in COVID-19. Our data also suggest a possible causative role of EC senescence in the aggravated disease in elder COVID-19 patients. Twit Text FOAVip Senescent endothelial cells are predisposed to SARS-CoV-2 infection and subsequent endothelial dysfunction ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=35879338 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35879338 #FOAvip English Wikipedia <ref>{{Cite pmid|35879338}}</ref> Senescent endothelial cells are predisposed to SARS-CoV-2 infection and subsequent endothelial dysfunction #MMPMID35879338 Urata R; Ikeda K; Yamazaki E; Ueno D; Katayama A; Shin-Ya M; Ohgitani E; Mazda O; Matoba S Sci Rep 2022[Jul]; 12 (1): 11855 PMID35879338show ga The coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains to spread worldwide. COVID-19 is characterized by the striking high mortality in elderly; however, its mechanistic insights remain unclear. Systemic thrombosis has been highlighted in the pathogenesis of COVID-19, and lung microangiopathy in association with endothelial cells (ECs) injury has been reported by post-mortem analysis of the lungs. Here, we experimentally investigated the SARS-CoV-2 infection in cultured human ECs, and performed a comparative analysis for post-infection molecular events using early passage and replicative senescent ECs. We found that; (1) SARS-CoV-2 infects ECs but does not replicate and disappears in 72 hours without causing severe cell damage, (2) Senescent ECs are highly susceptible to SARS-CoV-2 infection, (3) SARS-CoV-2 infection alters various genes expression, which could cause EC dysfunctions, (4) More genes expression is affected in senescent ECs by SARS-CoV-2 infection than in early passage ECs, which might causes further exacerbated dysfunction in senescent ECs. These data suggest that sustained EC dysfunctions due to SARS-CoV-2 infection may contribute to the microangiopathy in the lungs, leading to deteriorated inflammation and thrombosis in COVID-19. Our data also suggest a possible causative role of EC senescence in the aggravated disease in elder COVID-19 patients. |*COVID-19[MESH] |*Thrombosis/pathology[MESH] |Aged[MESH] |Disease Susceptibility/metabolism[MESH] |Endothelial Cells/metabolism[MESH] |Humans[MESH]Senescent endothelial cells are predisposed to SARS-CoV-2 infection an(epmc).pdf DeepDyve Pubget Overpricing