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10.3390/ijms23031911 http://scihub22266oqcxt.onion/10.3390/ijms23031911 35163833!8836815!35163833     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Mol+Sci 2022 ; 23 (3): ä Nephropedia Template TP {{tp|p=35163833|t=2022. AKR1B10, One of the Triggers of Cytokine Storm in SARS-CoV2 Severe Acute Respiratory Syndrome |pdf=|usr=}}{{35163833}} gab.com Text AKR1B10, One of the Triggers of Cytokine Storm in SARS-CoV2 Severe Acute Respiratory Syndrome JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=35163833 #FOAvip Preventing the cytokine storm observed in COVID-19 is a crucial goal for reducing the occurrence of severe acute respiratory failure and improving outcomes. Here, we identify Aldo-Keto Reductase 1B10 (AKR1B10) as a key enzyme involved in the expression of pro-inflammatory cytokines. The analysis of transcriptomic data from lung samples of patients who died from COVID-19 demonstrates an increased expression of the gene encoding AKR1B10. Measurements of the AKR1B10 protein in sera from hospitalised COVID-19 patients suggests a significant link between AKR1B10 levels and the severity of the disease. In macrophages and lung cells, the over-expression of AKR1B10 induces the expression of the pro-inflammatory cytokines Interleukin-6 (IL-6), Interleukin-1beta (IL-1beta) and Tumor Necrosis Factor a (TNFalpha), supporting the biological plausibility of an AKR1B10 involvement in the COVID-19-related cytokine storm. When macrophages were stressed by lipopolysaccharides (LPS) exposure and treated by Zopolrestat, an AKR1B10 inhibitor, the LPS-induced production of IL-6, IL-1beta, and TNFalpha is significantly reduced, reinforcing the hypothesis that the pro-inflammatory expression of cytokines is AKR1B10-dependant. Finally, we also show that AKR1B10 can be secreted and transferred via extracellular vesicles between different cell types, suggesting that this protein may also contribute to the multi-organ systemic impact of COVID-19. These experiments highlight a relationship between AKR1B10 production and severe forms of COVID-19. Our data indicate that AKR1B10 participates in the activation of cytokines production and suggest that modulation of AKR1B10 activity might be an actionable pharmacological target in COVID-19 management. Twit Text FOAVip AKR1B10, One of the Triggers of Cytokine Storm in SARS-CoV2 Severe Acute Respiratory Syndrome ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=35163833 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35163833 #FOAvip English Wikipedia <ref>{{Cite pmid|35163833}}</ref> AKR1B10, One of the Triggers of Cytokine Storm in SARS-CoV2 Severe Acute Respiratory Syndrome #MMPMID35163833 Chabert C; Vitte AL; Iuso D; Chuffart F; Trocme C; Buisson M; Poignard P; Lardinois B; Debois R; Rousseaux S; Pepin JL; Martinot JB; Khochbin S Int J Mol Sci 2022[Feb]; 23 (3): ä PMID35163833show ga Preventing the cytokine storm observed in COVID-19 is a crucial goal for reducing the occurrence of severe acute respiratory failure and improving outcomes. Here, we identify Aldo-Keto Reductase 1B10 (AKR1B10) as a key enzyme involved in the expression of pro-inflammatory cytokines. The analysis of transcriptomic data from lung samples of patients who died from COVID-19 demonstrates an increased expression of the gene encoding AKR1B10. Measurements of the AKR1B10 protein in sera from hospitalised COVID-19 patients suggests a significant link between AKR1B10 levels and the severity of the disease. In macrophages and lung cells, the over-expression of AKR1B10 induces the expression of the pro-inflammatory cytokines Interleukin-6 (IL-6), Interleukin-1beta (IL-1beta) and Tumor Necrosis Factor a (TNFalpha), supporting the biological plausibility of an AKR1B10 involvement in the COVID-19-related cytokine storm. When macrophages were stressed by lipopolysaccharides (LPS) exposure and treated by Zopolrestat, an AKR1B10 inhibitor, the LPS-induced production of IL-6, IL-1beta, and TNFalpha is significantly reduced, reinforcing the hypothesis that the pro-inflammatory expression of cytokines is AKR1B10-dependant. Finally, we also show that AKR1B10 can be secreted and transferred via extracellular vesicles between different cell types, suggesting that this protein may also contribute to the multi-organ systemic impact of COVID-19. These experiments highlight a relationship between AKR1B10 production and severe forms of COVID-19. Our data indicate that AKR1B10 participates in the activation of cytokines production and suggest that modulation of AKR1B10 activity might be an actionable pharmacological target in COVID-19 management. |Aldo-Keto Reductases/antagonists & inhibitors/genetics/*physiology[MESH] |Animals[MESH] |COVID-19/complications/*genetics/metabolism/pathology[MESH] |Case-Control Studies[MESH] |Cells, Cultured[MESH] |Cytokine Release Syndrome/*genetics/metabolism/pathology/virology[MESH] |Cytokines/metabolism[MESH] |Enzyme Inhibitors/pharmacology[MESH] |Humans[MESH] |Macrophages/drug effects/metabolism[MESH] |Mice[MESH] |Patient Acuity[MESH] |RAW 264.7 Cells[MESH] |Respiratory Distress Syndrome/*genetics/metabolism/pathology/virology[MESH] |SARS-CoV-2/physiology[MESH]AKR1B10, One of the Triggers of Cytokine Storm in SARS-CoV2 Severe Acu(epmc).pdf DeepDyve Pubget Overpricing