PMC:7161517 / 31944-33323 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T195","span":{"begin":743,"end":748},"obj":"Body_part"},{"id":"T196","span":{"begin":832,"end":837},"obj":"Body_part"},{"id":"T197","span":{"begin":851,"end":856},"obj":"Body_part"},{"id":"T198","span":{"begin":1059,"end":1065},"obj":"Body_part"}],"attributes":[{"id":"A195","pred":"fma_id","subj":"T195","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A196","pred":"fma_id","subj":"T196","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A197","pred":"fma_id","subj":"T197","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A198","pred":"fma_id","subj":"T198","obj":"http://purl.org/sig/ont/fma/fma9637"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T85","span":{"begin":743,"end":748},"obj":"Body_part"},{"id":"T86","span":{"begin":832,"end":837},"obj":"Body_part"},{"id":"T87","span":{"begin":851,"end":856},"obj":"Body_part"},{"id":"T88","span":{"begin":958,"end":961},"obj":"Body_part"},{"id":"T89","span":{"begin":1059,"end":1065},"obj":"Body_part"},{"id":"T90","span":{"begin":1248,"end":1251},"obj":"Body_part"},{"id":"T91","span":{"begin":1323,"end":1326},"obj":"Body_part"}],"attributes":[{"id":"A85","pred":"uberon_id","subj":"T85","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A86","pred":"uberon_id","subj":"T86","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A87","pred":"uberon_id","subj":"T87","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A88","pred":"uberon_id","subj":"T88","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"},{"id":"A89","pred":"uberon_id","subj":"T89","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A90","pred":"uberon_id","subj":"T90","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"},{"id":"A91","pred":"uberon_id","subj":"T91","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T176","span":{"begin":3,"end":11},"obj":"Disease"},{"id":"T177","span":{"begin":335,"end":347},"obj":"Disease"},{"id":"T178","span":{"begin":387,"end":395},"obj":"Disease"},{"id":"T179","span":{"begin":422,"end":444},"obj":"Disease"},{"id":"T180","span":{"begin":449,"end":457},"obj":"Disease"},{"id":"T181","span":{"begin":743,"end":756},"obj":"Disease"},{"id":"T182","span":{"begin":851,"end":864},"obj":"Disease"},{"id":"T183","span":{"begin":1107,"end":1115},"obj":"Disease"},{"id":"T184","span":{"begin":1133,"end":1155},"obj":"Disease"},{"id":"T185","span":{"begin":1222,"end":1230},"obj":"Disease"},{"id":"T186","span":{"begin":1370,"end":1378},"obj":"Disease"}],"attributes":[{"id":"A176","pred":"mondo_id","subj":"T176","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A177","pred":"mondo_id","subj":"T177","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A178","pred":"mondo_id","subj":"T178","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A179","pred":"mondo_id","subj":"T179","obj":"http://purl.obolibrary.org/obo/MONDO_0004995"},{"id":"A180","pred":"mondo_id","subj":"T180","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A181","pred":"mondo_id","subj":"T181","obj":"http://purl.obolibrary.org/obo/MONDO_0005252"},{"id":"A182","pred":"mondo_id","subj":"T182","obj":"http://purl.obolibrary.org/obo/MONDO_0005252"},{"id":"A183","pred":"mondo_id","subj":"T183","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A184","pred":"mondo_id","subj":"T184","obj":"http://purl.obolibrary.org/obo/MONDO_0004995"},{"id":"A185","pred":"mondo_id","subj":"T185","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A186","pred":"mondo_id","subj":"T186","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T308","span":{"begin":29,"end":37},"obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"T309","span":{"begin":522,"end":523},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T310","span":{"begin":566,"end":567},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T311","span":{"begin":743,"end":748},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T312","span":{"begin":743,"end":748},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T313","span":{"begin":743,"end":748},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T314","span":{"begin":743,"end":748},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T315","span":{"begin":832,"end":837},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T316","span":{"begin":832,"end":837},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T317","span":{"begin":832,"end":837},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T318","span":{"begin":832,"end":837},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T319","span":{"begin":851,"end":856},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T320","span":{"begin":851,"end":856},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T321","span":{"begin":851,"end":856},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T322","span":{"begin":851,"end":856},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T323","span":{"begin":1016,"end":1017},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T334","span":{"begin":472,"end":486},"obj":"Chemical"},{"id":"T335","span":{"begin":476,"end":486},"obj":"Chemical"},{"id":"T336","span":{"begin":958,"end":961},"obj":"Chemical"},{"id":"T337","span":{"begin":962,"end":973},"obj":"Chemical"},{"id":"T338","span":{"begin":1248,"end":1251},"obj":"Chemical"},{"id":"T339","span":{"begin":1252,"end":1262},"obj":"Chemical"},{"id":"T340","span":{"begin":1323,"end":1326},"obj":"Chemical"}],"attributes":[{"id":"A334","pred":"chebi_id","subj":"T334","obj":"http://purl.obolibrary.org/obo/CHEBI_35457"},{"id":"A335","pred":"chebi_id","subj":"T335","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A336","pred":"chebi_id","subj":"T336","obj":"http://purl.obolibrary.org/obo/CHEBI_63620"},{"id":"A337","pred":"chebi_id","subj":"T337","obj":"http://purl.obolibrary.org/obo/CHEBI_48706"},{"id":"A338","pred":"chebi_id","subj":"T338","obj":"http://purl.obolibrary.org/obo/CHEBI_63620"},{"id":"A339","pred":"chebi_id","subj":"T339","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A340","pred":"chebi_id","subj":"T340","obj":"http://purl.obolibrary.org/obo/CHEBI_63620"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T87","span":{"begin":250,"end":260},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T88","span":{"begin":335,"end":347},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

{"project":"LitCovid-sentences","denotations":[{"id":"T194","span":{"begin":0,"end":398},"obj":"Sentence"},{"id":"T195","span":{"begin":399,"end":757},"obj":"Sentence"},{"id":"T196","span":{"begin":758,"end":1156},"obj":"Sentence"},{"id":"T197","span":{"begin":1157,"end":1379},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T49","span":{"begin":422,"end":444},"obj":"Phenotype"},{"id":"T50","span":{"begin":743,"end":756},"obj":"Phenotype"},{"id":"T51","span":{"begin":851,"end":864},"obj":"Phenotype"},{"id":"T52","span":{"begin":1133,"end":1155},"obj":"Phenotype"}],"attributes":[{"id":"A49","pred":"hp_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/HP_0001626"},{"id":"A50","pred":"hp_id","subj":"T50","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A51","pred":"hp_id","subj":"T51","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A52","pred":"hp_id","subj":"T52","obj":"http://purl.obolibrary.org/obo/HP_0001626"}],"text":"If SARS-CoV-2 down-regulates membrane-bound ACE2 by promoting the ADAM17−mediated ectodomain shedding, resulting in increased concentrations of soluble ACE2 without compromising viral propagation, we hypothesize this would result in the overall down regulation of the ACE2/Ang1-7/Mas pathway, which would contribute to the severity of inflammation and systemic dysregulation observed in SARS-CoV-2. Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

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Thus, in patients with cardiovascular disease and SARS-CoV-2, the use of ACE inhibitors, ARBs, or MRAs may be favorable as a method to endogenously upregulate ACE2 as a compensatory mechanism that provides anti-inflammatory, antifibrotic, and antithrombotic support as well as reduction in progression of vascular and/or cardiac remodeling and heart failure. Several societies, including the American College of Cardiology, American Heart Association, Heart Failure Society of America (68), and European Society of Cardiology (69) have recommended continuing RAS antagonists because of the lack of conclusive data on a link between upregulation of systemic or tissue ACE2 and the increased susceptibility to COVID-19 in patients with cardiovascular disease. Based on our review, we hypothesize cardiovascular patients with COVID-19 should remain on RAS inhibitors because of the protective effects of the ACE2 pathway until RAS blockade is proven to increase the risk of COVID-19."}

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