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10.1007/s11739-020-02348-6 http://scihub22266oqcxt.onion/10.1007/s11739-020-02348-6 32399954!7214847!32399954     free     free     free       Intern+Emerg+Med 2020 ; 15 (5): 755-758 Nephropedia Template TP {{tp|p=32399954|t=2020. SARS-CoV-2 and myocardial injury: a role for Nox2?|pdf=|usr=}}{{32399954}} gab.com Text SARS-CoV-2 and myocardial injury: a role for Nox2 JO: Intern Emerg Med http://www.kidney.de/pget.php?&tw=1&pmid=32399954 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may be complicated by myocardial injury but at-risk patients as well as mechanism of disease are unclear. We gathered data regarding troponin levels in the so far reported SARS-CoV-2 patients and found a large variability in terms of troponin levels, patients with more severe disease, as those treated by ICU, presenting with higher percentage of troponin elevation. However, lack of prospective studies hampers adequate analysis of risk factors of myocardial damage. Previous study demonstrated that Nox2 is up-regulated in pneumonia and closely associated with troponin elevation suggesting Nox2 activation as mechanism eliciting myocardial damage; data in SARS-CoV-2 are still lacking. We hypothesize that SARS-Cov-2 may induce myocardial injury via Nox2-related ROS production and that analysis and eventually targeting Nox2 may be a novel approach to manage SARS-CoV-2. Twit Text FOAVip SARS-CoV-2 and myocardial injury: a role for Nox2 ????Intern Emerg Med http://www.kidney.de/pget.php?&tw=1&pmid=32399954 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32399954 #FOAvip English Wikipedia <ref>{{Cite pmid|32399954}}</ref> SARS-CoV-2 and myocardial injury: a role for Nox2? #MMPMID32399954 Violi F; Pastori D; Pignatelli P; Cangemi R Intern Emerg Med 2020[Aug]; 15 (5): 755-758 PMID32399954show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may be complicated by myocardial injury but at-risk patients as well as mechanism of disease are unclear. We gathered data regarding troponin levels in the so far reported SARS-CoV-2 patients and found a large variability in terms of troponin levels, patients with more severe disease, as those treated by ICU, presenting with higher percentage of troponin elevation. However, lack of prospective studies hampers adequate analysis of risk factors of myocardial damage. Previous study demonstrated that Nox2 is up-regulated in pneumonia and closely associated with troponin elevation suggesting Nox2 activation as mechanism eliciting myocardial damage; data in SARS-CoV-2 are still lacking. We hypothesize that SARS-Cov-2 may induce myocardial injury via Nox2-related ROS production and that analysis and eventually targeting Nox2 may be a novel approach to manage SARS-CoV-2. |Betacoronavirus[MESH] |Biomarkers/blood[MESH] |COVID-19[MESH] |Coronavirus Infections/*complications[MESH] |Heart Diseases/blood/*virology[MESH] |Humans[MESH] |Pandemics[MESH] |Pneumonia, Viral/*complications[MESH] |Prognosis[MESH] |SARS-CoV-2[MESH]SARS-CoV-2 and myocardial injury: a role for Nox2?(epmc).pdf DeepDyve Pubget Overpricing