PMC:7161517 / 8104-8405 JSONTXT

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T96","span":{"begin":126,"end":135},"obj":"http://purl.obolibrary.org/obo/SO_0000418"}],"text":"The treatment of ACE2 knockout mice with Ang II infusion and recombinant ACE2 (rhACE2) eliminated ERK1/2, JAK2-STAT3, and PKC signaling by rhACE2 and was at least partially responsible for attenuation of Ang II−induced myocardial hypertrophy and fibrosis and improvement in diastolic dysfunction (33)."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T82","span":{"begin":45,"end":47},"obj":"Chemical"},{"id":"T83","span":{"begin":208,"end":210},"obj":"Chemical"}],"attributes":[{"id":"A82","pred":"chebi_id","subj":"T82","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A83","pred":"chebi_id","subj":"T83","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"}],"text":"The treatment of ACE2 knockout mice with Ang II infusion and recombinant ACE2 (rhACE2) eliminated ERK1/2, JAK2-STAT3, and PKC signaling by rhACE2 and was at least partially responsible for attenuation of Ang II−induced myocardial hypertrophy and fibrosis and improvement in diastolic dysfunction (33)."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T27","span":{"begin":98,"end":102},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T28","span":{"begin":126,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0023052"}],"text":"The treatment of ACE2 knockout mice with Ang II infusion and recombinant ACE2 (rhACE2) eliminated ERK1/2, JAK2-STAT3, and PKC signaling by rhACE2 and was at least partially responsible for attenuation of Ang II−induced myocardial hypertrophy and fibrosis and improvement in diastolic dysfunction (33)."}

{"project":"LitCovid-sentences","denotations":[{"id":"T56","span":{"begin":0,"end":301},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"The treatment of ACE2 knockout mice with Ang II infusion and recombinant ACE2 (rhACE2) eliminated ERK1/2, JAK2-STAT3, and PKC signaling by rhACE2 and was at least partially responsible for attenuation of Ang II−induced myocardial hypertrophy and fibrosis and improvement in diastolic dysfunction (33)."}

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{"project":"2_test","denotations":[{"id":"32305401-20679547-55252939","span":{"begin":297,"end":299},"obj":"20679547"}],"text":"The treatment of ACE2 knockout mice with Ang II infusion and recombinant ACE2 (rhACE2) eliminated ERK1/2, JAK2-STAT3, and PKC signaling by rhACE2 and was at least partially responsible for attenuation of Ang II−induced myocardial hypertrophy and fibrosis and improvement in diastolic dysfunction (33)."}