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10.1016/j.yjmcc.2020.05.007 http://scihub22266oqcxt.onion/10.1016/j.yjmcc.2020.05.007 32422320!7228886!32422320     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 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\32422320.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Mol+Cell+Cardiol 2020 ; 144 (ä): 63-65 Nephropedia Template TP {{tp|p=32422320|t=2020. p38 MAPK inhibition: A promising therapeutic approach for COVID-19 |pdf=|usr=}}{{32422320}} gab.com Text p38 MAPK inhibition: A promising therapeutic approach for COVID-19 JO: J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=32422320 #FOAvip COVID-19, caused by the SARS-CoV-2 virus, is a major source of morbidity and mortality due to its inflammatory effects in the lungs and heart. The p38 MAPK pathway plays a crucial role in the release of pro-inflammatory cytokines such as IL-6 and has been implicated in acute lung injury and myocardial dysfunction. The overwhelming inflammatory response in COVID-19 infection may be caused by disproportionately upregulated p38 activity, explained by two mechanisms. First, angiotensin-converting enzyme 2 (ACE2) activity is lost during SARS-CoV-2 viral entry. ACE2 is highly expressed in the lungs and heart and converts Angiotensin II into Angiotensin 1-7. Angiotensin II signals proinflammatory, pro-vasoconstrictive, pro-thrombotic activity through p38 MAPK activation, which is countered by Angiotensin 1-7 downregulation of p38 activity. Loss of ACE2 upon viral entry may tip the balance towards destructive p38 signaling through Angiotensin II. Second, SARS-CoV was previously shown to directly upregulate p38 activity via a viral protein, similar to other RNA respiratory viruses that may hijack p38 activity to promote replication. Given the homology between SARS-CoV and SARS-CoV-2, the latter may employ a similar mechanism. Thus, SARS-CoV-2 may induce overwhelming inflammation by directly activating p38 and downregulating a key inhibitory pathway, while simultaneously taking advantage of p38 activity to replicate. Therapeutic inhibition of p38 could therefore attenuate COVID-19 infection. Interestingly, a prior preclinical study showed protective effects of p38 inhibition in a SARS-CoV mouse model. A number of p38 inhibitors are in the clinical stage and should be considered for clinical trials in serious COVID-19 infection. Twit Text FOAVip p38 MAPK inhibition: A promising therapeutic approach for COVID-19 ????J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=32422320 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32422320 #FOAvip English Wikipedia <ref>{{Cite pmid|32422320}}</ref> p38 MAPK inhibition: A promising therapeutic approach for COVID-19 #MMPMID32422320 Grimes JM; Grimes KV J Mol Cell Cardiol 2020[Jul]; 144 (ä): 63-65 PMID32422320show ga COVID-19, caused by the SARS-CoV-2 virus, is a major source of morbidity and mortality due to its inflammatory effects in the lungs and heart. The p38 MAPK pathway plays a crucial role in the release of pro-inflammatory cytokines such as IL-6 and has been implicated in acute lung injury and myocardial dysfunction. The overwhelming inflammatory response in COVID-19 infection may be caused by disproportionately upregulated p38 activity, explained by two mechanisms. First, angiotensin-converting enzyme 2 (ACE2) activity is lost during SARS-CoV-2 viral entry. ACE2 is highly expressed in the lungs and heart and converts Angiotensin II into Angiotensin 1-7. Angiotensin II signals proinflammatory, pro-vasoconstrictive, pro-thrombotic activity through p38 MAPK activation, which is countered by Angiotensin 1-7 downregulation of p38 activity. Loss of ACE2 upon viral entry may tip the balance towards destructive p38 signaling through Angiotensin II. Second, SARS-CoV was previously shown to directly upregulate p38 activity via a viral protein, similar to other RNA respiratory viruses that may hijack p38 activity to promote replication. Given the homology between SARS-CoV and SARS-CoV-2, the latter may employ a similar mechanism. Thus, SARS-CoV-2 may induce overwhelming inflammation by directly activating p38 and downregulating a key inhibitory pathway, while simultaneously taking advantage of p38 activity to replicate. Therapeutic inhibition of p38 could therefore attenuate COVID-19 infection. Interestingly, a prior preclinical study showed protective effects of p38 inhibition in a SARS-CoV mouse model. A number of p38 inhibitors are in the clinical stage and should be considered for clinical trials in serious COVID-19 infection. |Animals[MESH] |Antiviral Agents/*pharmacology[MESH] |Betacoronavirus/pathogenicity[MESH] |COVID-19[MESH] |COVID-19 Drug Treatment[MESH] |Coronavirus Infections/*drug therapy/enzymology[MESH] |Enzyme Activation[MESH] |Host-Pathogen Interactions/physiology[MESH] |Humans[MESH] |Inflammation/drug therapy/virology[MESH] |Lung/metabolism/physiopathology/virology[MESH] |Pandemics[MESH] |Pneumonia, Viral/*drug therapy/enzymology[MESH] |Protein Kinase Inhibitors/*pharmacology[MESH] |SARS-CoV-2[MESH]p38 MAPK inhibition: A promising therapeutic approach for COVID-19 (epmc).pdf DeepDyve Pubget Overpricing