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10.1038/s41392-021-00690-5 http://scihub22266oqcxt.onion/10.1038/s41392-021-00690-5 34253708!8273371!34253708     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34253708&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 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Signal+Transduct+Target+Ther 2021 ; 6 (1): 266 Nephropedia Template TP {{tp|p=34253708|t=2021. The zinc finger transcription factor, KLF2, protects against COVID-19 associated endothelial dysfunction |pdf=|usr=}}{{34253708}} gab.com Text The zinc finger transcription factor, KLF2, protects against COVID-19 associated endothelial dysfunction JO: Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=34253708 #FOAvip Coronavirus disease 2019 (COVID-19) is regarded as an endothelial disease (endothelialitis) with its patho-mechanism being incompletely understood. Emerging evidence has demonstrated that endothelial dysfunction precipitates COVID-19 and its accompanying multi-organ injuries. Thus, pharmacotherapies targeting endothelial dysfunction have potential to ameliorate COVID-19 and its cardiovascular complications. The objective of the present study is to evaluate whether kruppel-like factor 2 (KLF2), a master regulator of vascular homeostasis, represents a therapeutic target for COVID-19-induced endothelial dysfunction. Here, we demonstrate that the expression of KLF2 was reduced and monocyte adhesion was increased in endothelial cells treated with COVID-19 patient serum due to elevated levels of pro-adhesive molecules, ICAM1 and VCAM1. IL-1beta and TNF-alpha, two cytokines elevated in cytokine release syndrome in COVID-19 patients, decreased KLF2 gene expression. Pharmacologic (atorvastatin and tannic acid) and genetic (adenoviral overexpression) approaches to augment KLF2 levels attenuated COVID-19-serum-induced increase in endothelial inflammation and monocyte adhesion. Next-generation RNA-sequencing data showed that atorvastatin treatment leads to a cardiovascular protective transcriptome associated with improved endothelial function (vasodilation, anti-inflammation, antioxidant status, anti-thrombosis/-coagulation, anti-fibrosis, and reduced angiogenesis). Finally, knockdown of KLF2 partially reversed the ameliorative effect of atorvastatin on COVID-19-serum-induced endothelial inflammation and monocyte adhesion. Collectively, the present study implicates loss of KLF2 as an important molecular event in the development of COVID-19-induced vascular disease and suggests that efforts to augment KLF2 levels may be therapeutically beneficial. Twit Text FOAVip The zinc finger transcription factor, KLF2, protects against COVID-19 associated endothelial dysfunction ????Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=34253708 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34253708 #FOAvip English Wikipedia <ref>{{Cite pmid|34253708}}</ref> The zinc finger transcription factor, KLF2, protects against COVID-19 associated endothelial dysfunction #MMPMID34253708 Xu S; Liu Y; Ding Y; Luo S; Zheng X; Wu X; Liu Z; Ilyas I; Chen S; Han S; Little PJ; Jain MK; Weng J Signal Transduct Target Ther 2021[Jul]; 6 (1): 266 PMID34253708show ga Coronavirus disease 2019 (COVID-19) is regarded as an endothelial disease (endothelialitis) with its patho-mechanism being incompletely understood. Emerging evidence has demonstrated that endothelial dysfunction precipitates COVID-19 and its accompanying multi-organ injuries. Thus, pharmacotherapies targeting endothelial dysfunction have potential to ameliorate COVID-19 and its cardiovascular complications. The objective of the present study is to evaluate whether kruppel-like factor 2 (KLF2), a master regulator of vascular homeostasis, represents a therapeutic target for COVID-19-induced endothelial dysfunction. Here, we demonstrate that the expression of KLF2 was reduced and monocyte adhesion was increased in endothelial cells treated with COVID-19 patient serum due to elevated levels of pro-adhesive molecules, ICAM1 and VCAM1. IL-1beta and TNF-alpha, two cytokines elevated in cytokine release syndrome in COVID-19 patients, decreased KLF2 gene expression. Pharmacologic (atorvastatin and tannic acid) and genetic (adenoviral overexpression) approaches to augment KLF2 levels attenuated COVID-19-serum-induced increase in endothelial inflammation and monocyte adhesion. Next-generation RNA-sequencing data showed that atorvastatin treatment leads to a cardiovascular protective transcriptome associated with improved endothelial function (vasodilation, anti-inflammation, antioxidant status, anti-thrombosis/-coagulation, anti-fibrosis, and reduced angiogenesis). Finally, knockdown of KLF2 partially reversed the ameliorative effect of atorvastatin on COVID-19-serum-induced endothelial inflammation and monocyte adhesion. Collectively, the present study implicates loss of KLF2 as an important molecular event in the development of COVID-19-induced vascular disease and suggests that efforts to augment KLF2 levels may be therapeutically beneficial. |*COVID-19/genetics/metabolism/pathology/prevention & control[MESH] |*Human Umbilical Vein Endothelial Cells/metabolism/pathology/virology[MESH] |*SARS-CoV-2/genetics/metabolism[MESH] |Cytokines/biosynthesis/genetics[MESH] |Gene Expression Regulation[MESH] |Humans[MESH] |Intercellular Adhesion Molecule-1/biosynthesis/genetics[MESH] |Kruppel-Like Transcription Factors/*biosynthesis/genetics[MESH]The zinc finger transcription factor, KLF2, protects against COVID-19 (epmc).pdf DeepDyve Pubget Overpricing