PMC:7201239 / 765-2254 JSONTXT

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Humans are not equal with respect to the expression levels of the cellular ACE2. Moreover, ACE2 polymorphisms were recently described in human populations. Here we review the most recent evidence that ACE2 expression and/or polymorphism could influence both the susceptibility of people to SARS-CoV-2 infection and the outcome of the COVID-19 disease. Further exploration of the relationship between the virus, the peptidase function of ACE2 and the levels of angiotensin II in SARS-CoV-2 infected patients should help to better understand the pathophysiology of the disease and the multi-organ failures observed in severe COVID-19 cases, particularly heart failure.\n\nIntroduction\nOver the past 20 years, seven coronaviruses responsible for more or less severe respiratory diseases have emerged in humans. Several of them, including SARS-CoV-2 (a Betacoronavirus lineage b/Sarbecovirus), can cause patients lung injury and sometimes multi-organ failure with adverse myocardial remodeling, myocardial stress, and cardiomyopathy.1 , 2 Recently, SARS-CoV-2 was reported to be a human angiotensin I converting enzyme 2 (ACE2)-tropic virus3 , 4 able to bind the alveolar pneumocytes which express ACE2 at their surface.5 , 6 Yet, in humans the ACE2 mRNAs were found expressed in virtually all organs including the heart, blood vessels, kidney and testis, openi"}

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{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T15","span":{"begin":424,"end":432},"obj":"Disease"},{"id":"T16","span":{"begin":424,"end":428},"obj":"Disease"},{"id":"T17","span":{"begin":435,"end":444},"obj":"Disease"},{"id":"T18","span":{"begin":468,"end":476},"obj":"Disease"},{"id":"T19","span":{"begin":612,"end":620},"obj":"Disease"},{"id":"T20","span":{"begin":612,"end":616},"obj":"Disease"},{"id":"T21","span":{"begin":717,"end":737},"obj":"Disease"},{"id":"T22","span":{"begin":757,"end":765},"obj":"Disease"},{"id":"T23","span":{"begin":786,"end":799},"obj":"Disease"},{"id":"T24","span":{"begin":895,"end":915},"obj":"Disease"},{"id":"T25","span":{"begin":967,"end":975},"obj":"Disease"},{"id":"T26","span":{"begin":967,"end":971},"obj":"Disease"},{"id":"T27","span":{"begin":1046,"end":1052},"obj":"Disease"},{"id":"T28","span":{"begin":1067,"end":1086},"obj":"Disease"},{"id":"T29","span":{"begin":1134,"end":1160},"obj":"Disease"},{"id":"T30","span":{"begin":1146,"end":1160},"obj":"Disease"},{"id":"T31","span":{"begin":1177,"end":1185},"obj":"Disease"},{"id":"T32","span":{"begin":1177,"end":1181},"obj":"Disease"}],"attributes":[{"id":"A15","pred":"mondo_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A16","pred":"mondo_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A17","pred":"mondo_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A18","pred":"mondo_id","subj":"T18","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A19","pred":"mondo_id","subj":"T19","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A20","pred":"mondo_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A21","pred":"mondo_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/MONDO_0043726"},{"id":"A22","pred":"mondo_id","subj":"T22","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A23","pred":"mondo_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/MONDO_0005252"},{"id":"A24","pred":"mondo_id","subj":"T24","obj":"http://purl.obolibrary.org/obo/MONDO_0005087"},{"id":"A25","pred":"mondo_id","subj":"T25","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A26","pred":"mondo_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A27","pred":"mondo_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A28","pred":"mondo_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/MONDO_0043726"},{"id":"A29","pred":"mondo_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/MONDO_0019018"},{"id":"A30","pred":"mondo_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/MONDO_0004994"},{"id":"A31","pred":"mondo_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A32","pred":"mondo_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"}],"text":"ptidase expressed at the surface of lung epithelial cells and other tissues, that regulates the renin-angiotensin-aldosterone system. Humans are not equal with respect to the expression levels of the cellular ACE2. Moreover, ACE2 polymorphisms were recently described in human populations. Here we review the most recent evidence that ACE2 expression and/or polymorphism could influence both the susceptibility of people to SARS-CoV-2 infection and the outcome of the COVID-19 disease. Further exploration of the relationship between the virus, the peptidase function of ACE2 and the levels of angiotensin II in SARS-CoV-2 infected patients should help to better understand the pathophysiology of the disease and the multi-organ failures observed in severe COVID-19 cases, particularly heart failure.\n\nIntroduction\nOver the past 20 years, seven coronaviruses responsible for more or less severe respiratory diseases have emerged in humans. Several of them, including SARS-CoV-2 (a Betacoronavirus lineage b/Sarbecovirus), can cause patients lung injury and sometimes multi-organ failure with adverse myocardial remodeling, myocardial stress, and cardiomyopathy.1 , 2 Recently, SARS-CoV-2 was reported to be a human angiotensin I converting enzyme 2 (ACE2)-tropic virus3 , 4 able to bind the alveolar pneumocytes which express ACE2 at their surface.5 , 6 Yet, in humans the ACE2 mRNAs were found expressed in virtually all organs including the heart, blood vessels, kidney and testis, openi"}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T14","span":{"begin":36,"end":57},"obj":"http://purl.obolibrary.org/obo/CL_0000082"},{"id":"T15","span":{"begin":134,"end":140},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T16","span":{"begin":271,"end":276},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T17","span":{"begin":538,"end":543},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T18","span":{"begin":723,"end":728},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T19","span":{"begin":786,"end":791},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T20","span":{"begin":786,"end":791},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T21","span":{"begin":786,"end":791},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T22","span":{"begin":786,"end":791},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T23","span":{"begin":932,"end":938},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T24","span":{"begin":979,"end":980},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T25","span":{"begin":1005,"end":1006},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T26","span":{"begin":1041,"end":1045},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T27","span":{"begin":1041,"end":1045},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T28","span":{"begin":1073,"end":1078},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T29","span":{"begin":1207,"end":1208},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T30","span":{"begin":1209,"end":1214},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T31","span":{"begin":1362,"end":1368},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T32","span":{"begin":1422,"end":1428},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T33","span":{"begin":1443,"end":1448},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T34","span":{"begin":1443,"end":1448},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T35","span":{"begin":1443,"end":1448},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T36","span":{"begin":1443,"end":1448},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T37","span":{"begin":1450,"end":1463},"obj":"http://purl.obolibrary.org/obo/UBERON_0001981"},{"id":"T38","span":{"begin":1450,"end":1463},"obj":"http://www.ebi.ac.uk/efo/EFO_0000817"},{"id":"T39","span":{"begin":1465,"end":1471},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T40","span":{"begin":1465,"end":1471},"obj":"http://www.ebi.ac.uk/efo/EFO_0000927"},{"id":"T41","span":{"begin":1465,"end":1471},"obj":"http://www.ebi.ac.uk/efo/EFO_0000929"},{"id":"T42","span":{"begin":1476,"end":1482},"obj":"http://www.ebi.ac.uk/efo/EFO_0000984"}],"text":"ptidase expressed at the surface of lung epithelial cells and other tissues, that regulates the renin-angiotensin-aldosterone system. Humans are not equal with respect to the expression levels of the cellular ACE2. Moreover, ACE2 polymorphisms were recently described in human populations. Here we review the most recent evidence that ACE2 expression and/or polymorphism could influence both the susceptibility of people to SARS-CoV-2 infection and the outcome of the COVID-19 disease. Further exploration of the relationship between the virus, the peptidase function of ACE2 and the levels of angiotensin II in SARS-CoV-2 infected patients should help to better understand the pathophysiology of the disease and the multi-organ failures observed in severe COVID-19 cases, particularly heart failure.\n\nIntroduction\nOver the past 20 years, seven coronaviruses responsible for more or less severe respiratory diseases have emerged in humans. Several of them, including SARS-CoV-2 (a Betacoronavirus lineage b/Sarbecovirus), can cause patients lung injury and sometimes multi-organ failure with adverse myocardial remodeling, myocardial stress, and cardiomyopathy.1 , 2 Recently, SARS-CoV-2 was reported to be a human angiotensin I converting enzyme 2 (ACE2)-tropic virus3 , 4 able to bind the alveolar pneumocytes which express ACE2 at their surface.5 , 6 Yet, in humans the ACE2 mRNAs were found expressed in virtually all organs including the heart, blood vessels, kidney and testis, openi"}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T4","span":{"begin":102,"end":113},"obj":"Chemical"},{"id":"T5","span":{"begin":114,"end":125},"obj":"Chemical"},{"id":"T7","span":{"begin":594,"end":608},"obj":"Chemical"},{"id":"T10","span":{"begin":594,"end":605},"obj":"Chemical"},{"id":"T11","span":{"begin":606,"end":608},"obj":"Chemical"},{"id":"T12","span":{"begin":1215,"end":1226},"obj":"Chemical"}],"attributes":[{"id":"A4","pred":"chebi_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CHEBI_48433"},{"id":"A5","pred":"chebi_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_27584"},{"id":"A6","pred":"chebi_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_30834"},{"id":"A7","pred":"chebi_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A8","pred":"chebi_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_48432"},{"id":"A9","pred":"chebi_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_58506"},{"id":"A10","pred":"chebi_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/CHEBI_48433"},{"id":"A11","pred":"chebi_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A12","pred":"chebi_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/CHEBI_48433"}],"text":"ptidase expressed at the surface of lung epithelial cells and other tissues, that regulates the renin-angiotensin-aldosterone system. Humans are not equal with respect to the expression levels of the cellular ACE2. Moreover, ACE2 polymorphisms were recently described in human populations. Here we review the most recent evidence that ACE2 expression and/or polymorphism could influence both the susceptibility of people to SARS-CoV-2 infection and the outcome of the COVID-19 disease. Further exploration of the relationship between the virus, the peptidase function of ACE2 and the levels of angiotensin II in SARS-CoV-2 infected patients should help to better understand the pathophysiology of the disease and the multi-organ failures observed in severe COVID-19 cases, particularly heart failure.\n\nIntroduction\nOver the past 20 years, seven coronaviruses responsible for more or less severe respiratory diseases have emerged in humans. Several of them, including SARS-CoV-2 (a Betacoronavirus lineage b/Sarbecovirus), can cause patients lung injury and sometimes multi-organ failure with adverse myocardial remodeling, myocardial stress, and cardiomyopathy.1 , 2 Recently, SARS-CoV-2 was reported to be a human angiotensin I converting enzyme 2 (ACE2)-tropic virus3 , 4 able to bind the alveolar pneumocytes which express ACE2 at their surface.5 , 6 Yet, in humans the ACE2 mRNAs were found expressed in virtually all organs including the heart, blood vessels, kidney and testis, openi"}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T2","span":{"begin":786,"end":799},"obj":"Phenotype"},{"id":"T3","span":{"begin":1146,"end":1160},"obj":"Phenotype"}],"attributes":[{"id":"A2","pred":"hp_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/HP_0001638"}],"text":"ptidase expressed at the surface of lung epithelial cells and other tissues, that regulates the renin-angiotensin-aldosterone system. Humans are not equal with respect to the expression levels of the cellular ACE2. Moreover, ACE2 polymorphisms were recently described in human populations. Here we review the most recent evidence that ACE2 expression and/or polymorphism could influence both the susceptibility of people to SARS-CoV-2 infection and the outcome of the COVID-19 disease. Further exploration of the relationship between the virus, the peptidase function of ACE2 and the levels of angiotensin II in SARS-CoV-2 infected patients should help to better understand the pathophysiology of the disease and the multi-organ failures observed in severe COVID-19 cases, particularly heart failure.\n\nIntroduction\nOver the past 20 years, seven coronaviruses responsible for more or less severe respiratory diseases have emerged in humans. Several of them, including SARS-CoV-2 (a Betacoronavirus lineage b/Sarbecovirus), can cause patients lung injury and sometimes multi-organ failure with adverse myocardial remodeling, myocardial stress, and cardiomyopathy.1 , 2 Recently, SARS-CoV-2 was reported to be a human angiotensin I converting enzyme 2 (ACE2)-tropic virus3 , 4 able to bind the alveolar pneumocytes which express ACE2 at their surface.5 , 6 Yet, in humans the ACE2 mRNAs were found expressed in virtually all organs including the heart, blood vessels, kidney and testis, openi"}

{"project":"LitCovid-sentences","denotations":[{"id":"T8","span":{"begin":134,"end":214},"obj":"Sentence"},{"id":"T9","span":{"begin":215,"end":289},"obj":"Sentence"},{"id":"T10","span":{"begin":290,"end":485},"obj":"Sentence"},{"id":"T11","span":{"begin":486,"end":800},"obj":"Sentence"},{"id":"T12","span":{"begin":802,"end":814},"obj":"Sentence"},{"id":"T13","span":{"begin":815,"end":939},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"ptidase expressed at the surface of lung epithelial cells and other tissues, that regulates the renin-angiotensin-aldosterone system. Humans are not equal with respect to the expression levels of the cellular ACE2. Moreover, ACE2 polymorphisms were recently described in human populations. Here we review the most recent evidence that ACE2 expression and/or polymorphism could influence both the susceptibility of people to SARS-CoV-2 infection and the outcome of the COVID-19 disease. Further exploration of the relationship between the virus, the peptidase function of ACE2 and the levels of angiotensin II in SARS-CoV-2 infected patients should help to better understand the pathophysiology of the disease and the multi-organ failures observed in severe COVID-19 cases, particularly heart failure.\n\nIntroduction\nOver the past 20 years, seven coronaviruses responsible for more or less severe respiratory diseases have emerged in humans. Several of them, including SARS-CoV-2 (a Betacoronavirus lineage b/Sarbecovirus), can cause patients lung injury and sometimes multi-organ failure with adverse myocardial remodeling, myocardial stress, and cardiomyopathy.1 , 2 Recently, SARS-CoV-2 was reported to be a human angiotensin I converting enzyme 2 (ACE2)-tropic virus3 , 4 able to bind the alveolar pneumocytes which express ACE2 at their surface.5 , 6 Yet, in humans the ACE2 mRNAs were found expressed in virtually all organs including the heart, blood vessels, kidney and testis, openi"}

{"project":"2_test","denotations":[{"id":"32414646-31978945-62239755","span":{"begin":1161,"end":1162},"obj":"31978945"},{"id":"32414646-31986264-62239756","span":{"begin":1165,"end":1166},"obj":"31986264"}],"text":"ptidase expressed at the surface of lung epithelial cells and other tissues, that regulates the renin-angiotensin-aldosterone system. Humans are not equal with respect to the expression levels of the cellular ACE2. Moreover, ACE2 polymorphisms were recently described in human populations. Here we review the most recent evidence that ACE2 expression and/or polymorphism could influence both the susceptibility of people to SARS-CoV-2 infection and the outcome of the COVID-19 disease. Further exploration of the relationship between the virus, the peptidase function of ACE2 and the levels of angiotensin II in SARS-CoV-2 infected patients should help to better understand the pathophysiology of the disease and the multi-organ failures observed in severe COVID-19 cases, particularly heart failure.\n\nIntroduction\nOver the past 20 years, seven coronaviruses responsible for more or less severe respiratory diseases have emerged in humans. Several of them, including SARS-CoV-2 (a Betacoronavirus lineage b/Sarbecovirus), can cause patients lung injury and sometimes multi-organ failure with adverse myocardial remodeling, myocardial stress, and cardiomyopathy.1 , 2 Recently, SARS-CoV-2 was reported to be a human angiotensin I converting enzyme 2 (ACE2)-tropic virus3 , 4 able to bind the alveolar pneumocytes which express ACE2 at their surface.5 , 6 Yet, in humans the ACE2 mRNAs were found expressed in virtually all organs including the heart, blood vessels, kidney and testis, openi"}