PMC:7352545 / 47495-48096 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T408","span":{"begin":511,"end":515},"obj":"Body_part"}],"attributes":[{"id":"A408","pred":"fma_id","subj":"T408","obj":"http://purl.org/sig/ont/fma/fma74402"}],"text":"Pulmonary ACE2 is potentially a candidate target in CoV-involved inflammatory pathogenesis. If ACE inhibitors and Ang II-AT1 blockers are dosed, ACE2 expression is increased. However, currently we have no conclusive evidence that the inhibitors help SARS-CoV or SARS-CoV-2 entry. Rather, SARS-CoV infection reduces ACE2 expression. Therefore, SARS-CoV-2 host tropism is not related to ACE2 expression. ACE2 levels and ANG II/ANG 1–7 levels regulate the pathogenic progression. ACE2 expression is upregulated by gene polymorphisms and ACE inhibitors or Angiotensin II receptor blockers such as sartans."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T161","span":{"begin":121,"end":124},"obj":"Disease"},{"id":"T162","span":{"begin":250,"end":258},"obj":"Disease"},{"id":"T163","span":{"begin":262,"end":270},"obj":"Disease"},{"id":"T164","span":{"begin":288,"end":306},"obj":"Disease"},{"id":"T165","span":{"begin":297,"end":306},"obj":"Disease"},{"id":"T166","span":{"begin":343,"end":351},"obj":"Disease"}],"attributes":[{"id":"A161","pred":"mondo_id","subj":"T161","obj":"http://purl.obolibrary.org/obo/MONDO_0008840"},{"id":"A162","pred":"mondo_id","subj":"T162","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A163","pred":"mondo_id","subj":"T163","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A164","pred":"mondo_id","subj":"T164","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A165","pred":"mondo_id","subj":"T165","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A166","pred":"mondo_id","subj":"T166","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"}],"text":"Pulmonary ACE2 is potentially a candidate target in CoV-involved inflammatory pathogenesis. If ACE inhibitors and Ang II-AT1 blockers are dosed, ACE2 expression is increased. However, currently we have no conclusive evidence that the inhibitors help SARS-CoV or SARS-CoV-2 entry. Rather, SARS-CoV infection reduces ACE2 expression. Therefore, SARS-CoV-2 host tropism is not related to ACE2 expression. ACE2 levels and ANG II/ANG 1–7 levels regulate the pathogenic progression. ACE2 expression is upregulated by gene polymorphisms and ACE inhibitors or Angiotensin II receptor blockers such as sartans."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T656","span":{"begin":30,"end":31},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T657","span":{"begin":511,"end":515},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"}],"text":"Pulmonary ACE2 is potentially a candidate target in CoV-involved inflammatory pathogenesis. If ACE inhibitors and Ang II-AT1 blockers are dosed, ACE2 expression is increased. However, currently we have no conclusive evidence that the inhibitors help SARS-CoV or SARS-CoV-2 entry. Rather, SARS-CoV infection reduces ACE2 expression. Therefore, SARS-CoV-2 host tropism is not related to ACE2 expression. ACE2 levels and ANG II/ANG 1–7 levels regulate the pathogenic progression. ACE2 expression is upregulated by gene polymorphisms and ACE inhibitors or Angiotensin II receptor blockers such as sartans."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T1466","span":{"begin":95,"end":109},"obj":"Chemical"},{"id":"T1467","span":{"begin":99,"end":109},"obj":"Chemical"},{"id":"T1468","span":{"begin":118,"end":120},"obj":"Chemical"},{"id":"T1469","span":{"begin":234,"end":244},"obj":"Chemical"},{"id":"T1470","span":{"begin":422,"end":424},"obj":"Chemical"},{"id":"T1471","span":{"begin":534,"end":548},"obj":"Chemical"},{"id":"T1472","span":{"begin":538,"end":548},"obj":"Chemical"},{"id":"T1473","span":{"begin":552,"end":566},"obj":"Chemical"},{"id":"T1474","span":{"begin":564,"end":566},"obj":"Chemical"}],"attributes":[{"id":"A1466","pred":"chebi_id","subj":"T1466","obj":"http://purl.obolibrary.org/obo/CHEBI_35457"},{"id":"A1467","pred":"chebi_id","subj":"T1467","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A1468","pred":"chebi_id","subj":"T1468","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A1469","pred":"chebi_id","subj":"T1469","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A1470","pred":"chebi_id","subj":"T1470","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A1471","pred":"chebi_id","subj":"T1471","obj":"http://purl.obolibrary.org/obo/CHEBI_35457"},{"id":"A1472","pred":"chebi_id","subj":"T1472","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A1473","pred":"chebi_id","subj":"T1473","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A1474","pred":"chebi_id","subj":"T1474","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"}],"text":"Pulmonary ACE2 is potentially a candidate target in CoV-involved inflammatory pathogenesis. If ACE inhibitors and Ang II-AT1 blockers are dosed, ACE2 expression is increased. However, currently we have no conclusive evidence that the inhibitors help SARS-CoV or SARS-CoV-2 entry. Rather, SARS-CoV infection reduces ACE2 expression. Therefore, SARS-CoV-2 host tropism is not related to ACE2 expression. ACE2 levels and ANG II/ANG 1–7 levels regulate the pathogenic progression. ACE2 expression is upregulated by gene polymorphisms and ACE inhibitors or Angiotensin II receptor blockers such as sartans."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T75","span":{"begin":78,"end":90},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T76","span":{"begin":359,"end":366},"obj":"http://purl.obolibrary.org/obo/GO_0009606"}],"text":"Pulmonary ACE2 is potentially a candidate target in CoV-involved inflammatory pathogenesis. If ACE inhibitors and Ang II-AT1 blockers are dosed, ACE2 expression is increased. However, currently we have no conclusive evidence that the inhibitors help SARS-CoV or SARS-CoV-2 entry. Rather, SARS-CoV infection reduces ACE2 expression. Therefore, SARS-CoV-2 host tropism is not related to ACE2 expression. ACE2 levels and ANG II/ANG 1–7 levels regulate the pathogenic progression. ACE2 expression is upregulated by gene polymorphisms and ACE inhibitors or Angiotensin II receptor blockers such as sartans."}

{"project":"LitCovid-sentences","denotations":[{"id":"T458","span":{"begin":0,"end":91},"obj":"Sentence"},{"id":"T459","span":{"begin":92,"end":174},"obj":"Sentence"},{"id":"T460","span":{"begin":175,"end":279},"obj":"Sentence"},{"id":"T461","span":{"begin":280,"end":331},"obj":"Sentence"},{"id":"T462","span":{"begin":332,"end":401},"obj":"Sentence"},{"id":"T463","span":{"begin":402,"end":476},"obj":"Sentence"},{"id":"T464","span":{"begin":477,"end":601},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Pulmonary ACE2 is potentially a candidate target in CoV-involved inflammatory pathogenesis. If ACE inhibitors and Ang II-AT1 blockers are dosed, ACE2 expression is increased. However, currently we have no conclusive evidence that the inhibitors help SARS-CoV or SARS-CoV-2 entry. Rather, SARS-CoV infection reduces ACE2 expression. Therefore, SARS-CoV-2 host tropism is not related to ACE2 expression. ACE2 levels and ANG II/ANG 1–7 levels regulate the pathogenic progression. ACE2 expression is upregulated by gene polymorphisms and ACE inhibitors or Angiotensin II receptor blockers such as sartans."}