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10.1016/j.cell.2021.03.026 http://scihub22266oqcxt.onion/10.1016/j.cell.2021.03.026 33811809!7962543!33811809     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       Cell 2021 ; 184 (8): 2167-2182.e22 Nephropedia Template TP {{tp|p=33811809|t=2021. BET inhibition blocks inflammation-induced cardiac dysfunction and SARS-CoV-2 infection |pdf=|usr=}}{{33811809}} gab.com Text BET inhibition blocks inflammation-induced cardiac dysfunction and SARS-CoV-2 infection JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=33811809 #FOAvip Cardiac injury and dysfunction occur in COVID-19 patients and increase the risk of mortality. Causes are ill defined but could be through direct cardiac infection and/or inflammation-induced dysfunction. To identify mechanisms and cardio-protective drugs, we use a state-of-the-art pipeline combining human cardiac organoids with phosphoproteomics and single nuclei RNA sequencing. We identify an inflammatory "cytokine-storm", a cocktail of interferon gamma, interleukin 1beta, and poly(I:C), induced diastolic dysfunction. Bromodomain-containing protein 4 is activated along with a viral response that is consistent in both human cardiac organoids (hCOs) and hearts of SARS-CoV-2-infected K18-hACE2 mice. Bromodomain and extraterminal family inhibitors (BETi) recover dysfunction in hCOs and completely prevent cardiac dysfunction and death in a mouse cytokine-storm model. Additionally, BETi decreases transcription of genes in the viral response, decreases ACE2 expression, and reduces SARS-CoV-2 infection of cardiomyocytes. Together, BETi, including the Food and Drug Administration (FDA) breakthrough designated drug, apabetalone, are promising candidates to prevent COVID-19 mediated cardiac damage. Twit Text FOAVip BET inhibition blocks inflammation-induced cardiac dysfunction and SARS-CoV-2 infection ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=33811809 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33811809 #FOAvip English Wikipedia <ref>{{Cite pmid|33811809}}</ref> BET inhibition blocks inflammation-induced cardiac dysfunction and SARS-CoV-2 infection #MMPMID33811809 Mills RJ; Humphrey SJ; Fortuna PRJ; Lor M; Foster SR; Quaife-Ryan GA; Johnston RL; Dumenil T; Bishop C; Rudraraju R; Rawle DJ; Le T; Zhao W; Lee L; Mackenzie-Kludas C; Mehdiabadi NR; Halliday C; Gilham D; Fu L; Nicholls SJ; Johansson J; Sweeney M; Wong NCW; Kulikowski E; Sokolowski KA; Tse BWC; Devilee L; Voges HK; Reynolds LT; Krumeich S; Mathieson E; Abu-Bonsrah D; Karavendzas K; Griffen B; Titmarsh D; Elliott DA; McMahon J; Suhrbier A; Subbarao K; Porrello ER; Smyth MJ; Engwerda CR; MacDonald KPA; Bald T; James DE; Hudson JE Cell 2021[Apr]; 184 (8): 2167-2182.e22 PMID33811809show ga Cardiac injury and dysfunction occur in COVID-19 patients and increase the risk of mortality. Causes are ill defined but could be through direct cardiac infection and/or inflammation-induced dysfunction. To identify mechanisms and cardio-protective drugs, we use a state-of-the-art pipeline combining human cardiac organoids with phosphoproteomics and single nuclei RNA sequencing. We identify an inflammatory "cytokine-storm", a cocktail of interferon gamma, interleukin 1beta, and poly(I:C), induced diastolic dysfunction. Bromodomain-containing protein 4 is activated along with a viral response that is consistent in both human cardiac organoids (hCOs) and hearts of SARS-CoV-2-infected K18-hACE2 mice. Bromodomain and extraterminal family inhibitors (BETi) recover dysfunction in hCOs and completely prevent cardiac dysfunction and death in a mouse cytokine-storm model. Additionally, BETi decreases transcription of genes in the viral response, decreases ACE2 expression, and reduces SARS-CoV-2 infection of cardiomyocytes. Together, BETi, including the Food and Drug Administration (FDA) breakthrough designated drug, apabetalone, are promising candidates to prevent COVID-19 mediated cardiac damage. |Angiotensin-Converting Enzyme 2/metabolism[MESH] |Animals[MESH] |COVID-19 Drug Treatment[MESH] |COVID-19/*complications[MESH] |Cardiotonic Agents/*therapeutic use[MESH] |Cell Cycle Proteins/*antagonists & inhibitors/metabolism[MESH] |Cell Line[MESH] |Cytokines/metabolism[MESH] |Female[MESH] |Heart Diseases/*drug therapy/etiology[MESH] |Human Embryonic Stem Cells[MESH] |Humans[MESH] |Inflammation/complications/drug therapy[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Quinazolinones/*therapeutic use[MESH]BET inhibition blocks inflammation-induced cardiac dysfunction and SAR(epmc).pdf DeepDyve Pubget Overpricing