PMC:7556165 / 25723-26689 JSONTXT

{"project":"LitCovid-sample-MedDRA","denotations":[{"id":"T61","span":{"begin":316,"end":328},"obj":"http://purl.bioontology.org/ontology/MEDDRA/10022891"},{"id":"T62","span":{"begin":395,"end":398},"obj":"http://purl.bioontology.org/ontology/MEDDRA/10022891"},{"id":"T63","span":{"begin":447,"end":461},"obj":"http://purl.bioontology.org/ontology/MEDDRA/10022891"},{"id":"T64","span":{"begin":755,"end":758},"obj":"http://purl.bioontology.org/ontology/MEDDRA/10022891"}],"attributes":[{"id":"A61","pred":"meddra_id","subj":"T61","obj":"http://purl.bioontology.org/ontology/MEDDRA/10062026"},{"id":"A63","pred":"meddra_id","subj":"T63","obj":"http://purl.bioontology.org/ontology/MEDDRA/10002491"},{"id":"A64","pred":"meddra_id","subj":"T64","obj":"http://purl.bioontology.org/ontology/MEDDRA/10050289"},{"id":"A62","pred":"meddra_id","subj":"T62","obj":"http://purl.bioontology.org/ontology/MEDDRA/10050289"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-CHEBI","denotations":[{"id":"T91","span":{"begin":447,"end":461},"obj":"Chemical"}],"attributes":[{"id":"A91","pred":"chebi_id","subj":"T91","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A92","pred":"chebi_id","subj":"T91","obj":"http://purl.obolibrary.org/obo/CHEBI_48432"},{"id":"A93","pred":"chebi_id","subj":"T91","obj":"http://purl.obolibrary.org/obo/CHEBI_58506"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-NCBITaxon","denotations":[{"id":"T77","span":{"begin":564,"end":569},"obj":"Species"}],"attributes":[{"id":"A77","pred":"ncbi_taxonomy_id","subj":"T77","obj":"NCBItxid:10090"},{"id":"A78","pred":"ncbi_taxonomy_id","subj":"T77","obj":"NCBItxid:10088"}],"namespaces":[{"prefix":"NCBItxid","uri":"http://purl.bioontology.org/ontology/NCBITAXON/"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-sentences","denotations":[{"id":"T165","span":{"begin":0,"end":264},"obj":"Sentence"},{"id":"T166","span":{"begin":265,"end":471},"obj":"Sentence"},{"id":"T167","span":{"begin":472,"end":698},"obj":"Sentence"},{"id":"T168","span":{"begin":699,"end":830},"obj":"Sentence"},{"id":"T169","span":{"begin":831,"end":966},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-UBERON","denotations":[{"id":"T114","span":{"begin":43,"end":48},"obj":"Body_part"},{"id":"T115","span":{"begin":53,"end":59},"obj":"Body_part"},{"id":"T116","span":{"begin":127,"end":133},"obj":"Body_part"},{"id":"T117","span":{"begin":893,"end":898},"obj":"Body_part"}],"attributes":[{"id":"A117","pred":"uberon_id","subj":"T117","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A114","pred":"uberon_id","subj":"T114","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A116","pred":"uberon_id","subj":"T116","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A115","pred":"uberon_id","subj":"T115","obj":"http://purl.obolibrary.org/obo/UBERON_0002113"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-Pubtator","denotations":[{"id":"688","span":{"begin":31,"end":35},"obj":"Gene"},{"id":"689","span":{"begin":150,"end":154},"obj":"Gene"},{"id":"690","span":{"begin":279,"end":283},"obj":"Gene"},{"id":"691","span":{"begin":373,"end":377},"obj":"Gene"},{"id":"692","span":{"begin":395,"end":398},"obj":"Gene"},{"id":"693","span":{"begin":447,"end":461},"obj":"Gene"},{"id":"694","span":{"begin":496,"end":500},"obj":"Gene"},{"id":"695","span":{"begin":577,"end":581},"obj":"Gene"},{"id":"696","span":{"begin":755,"end":758},"obj":"Gene"},{"id":"697","span":{"begin":861,"end":865},"obj":"Gene"},{"id":"698","span":{"begin":564,"end":569},"obj":"Species"},{"id":"699","span":{"begin":544,"end":554},"obj":"Species"}],"attributes":[{"id":"A693","pred":"pubann:denotes","subj":"693","obj":"Gene:183"},{"id":"A692","pred":"pubann:denotes","subj":"692","obj":"Gene:1636"},{"id":"A696","pred":"pubann:denotes","subj":"696","obj":"Gene:1636"},{"id":"A689","pred":"pubann:denotes","subj":"689","obj":"Gene:59272"},{"id":"A691","pred":"pubann:denotes","subj":"691","obj":"Gene:59272"},{"id":"A698","pred":"pubann:denotes","subj":"698","obj":"Tax:10090"},{"id":"A690","pred":"pubann:denotes","subj":"690","obj":"Gene:59272"},{"id":"A697","pred":"pubann:denotes","subj":"697","obj":"Gene:70008"},{"id":"A699","pred":"pubann:denotes","subj":"699","obj":"Tax:10090"},{"id":"A695","pred":"pubann:denotes","subj":"695","obj":"Gene:70008"},{"id":"A688","pred":"pubann:denotes","subj":"688","obj":"Gene:59272"},{"id":"A694","pred":"pubann:denotes","subj":"694","obj":"Gene:70008"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

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the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-IDO","denotations":[{"id":"T74","span":{"begin":893,"end":898},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-FMA","denotations":[{"id":"T248","span":{"begin":43,"end":48},"obj":"Body_part"},{"id":"T249","span":{"begin":53,"end":59},"obj":"Body_part"},{"id":"T250","span":{"begin":110,"end":117},"obj":"Body_part"},{"id":"T251","span":{"begin":127,"end":133},"obj":"Body_part"},{"id":"T252","span":{"begin":676,"end":697},"obj":"Body_part"},{"id":"T253","span":{"begin":893,"end":898},"obj":"Body_part"}],"attributes":[{"id":"A251","pred":"fma_id","subj":"T251","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A250","pred":"fma_id","subj":"T250","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A253","pred":"fma_id","subj":"T253","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A248","pred":"fma_id","subj":"T248","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A249","pred":"fma_id","subj":"T249","obj":"http://purl.org/sig/ont/fma/fma7203"},{"id":"A252","pred":"fma_id","subj":"T252","obj":"http://purl.org/sig/ont/fma/fma9556"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-MONDO","denotations":[{"id":"T61","span":{"begin":888,"end":907},"obj":"Disease"}],"attributes":[{"id":"A61","pred":"mondo_id","subj":"T61","obj":"http://purl.obolibrary.org/obo/MONDO_0005044"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-MAT","denotations":[{"id":"T99","span":{"begin":43,"end":48},"obj":"http://purl.obolibrary.org/obo/MAT_0000036"},{"id":"T100","span":{"begin":53,"end":59},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T101","span":{"begin":893,"end":898},"obj":"http://purl.obolibrary.org/obo/MAT_0000083"},{"id":"T102","span":{"begin":893,"end":898},"obj":"http://purl.obolibrary.org/obo/MAT_0000315"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-GO-BP-0","denotations":[{"id":"T66","span":{"begin":336,"end":346},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T67","span":{"begin":420,"end":436},"obj":"http://purl.obolibrary.org/obo/GO_0042310"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-PD-HP","denotations":[{"id":"T16","span":{"begin":888,"end":907},"obj":"Phenotype"}],"attributes":[{"id":"A16","pred":"hp_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/HP_0000822"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sample-GO-BP","denotations":[{"id":"T68","span":{"begin":336,"end":346},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T69","span":{"begin":420,"end":436},"obj":"http://purl.obolibrary.org/obo/GO_0042310"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T16","span":{"begin":888,"end":907},"obj":"Phenotype"}],"attributes":[{"id":"A16","pred":"hp_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/HP_0000822"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-PubTator","denotations":[{"id":"688","span":{"begin":31,"end":35},"obj":"Gene"},{"id":"689","span":{"begin":150,"end":154},"obj":"Gene"},{"id":"690","span":{"begin":279,"end":283},"obj":"Gene"},{"id":"691","span":{"begin":373,"end":377},"obj":"Gene"},{"id":"692","span":{"begin":395,"end":398},"obj":"Gene"},{"id":"693","span":{"begin":447,"end":461},"obj":"Gene"},{"id":"694","span":{"begin":496,"end":500},"obj":"Gene"},{"id":"695","span":{"begin":577,"end":581},"obj":"Gene"},{"id":"696","span":{"begin":755,"end":758},"obj":"Gene"},{"id":"697","span":{"begin":861,"end":865},"obj":"Gene"},{"id":"698","span":{"begin":564,"end":569},"obj":"Species"},{"id":"699","span":{"begin":544,"end":554},"obj":"Species"}],"attributes":[{"id":"A688","pred":"tao:has_database_id","subj":"688","obj":"Gene:59272"},{"id":"A689","pred":"tao:has_database_id","subj":"689","obj":"Gene:59272"},{"id":"A690","pred":"tao:has_database_id","subj":"690","obj":"Gene:59272"},{"id":"A691","pred":"tao:has_database_id","subj":"691","obj":"Gene:59272"},{"id":"A692","pred":"tao:has_database_id","subj":"692","obj":"Gene:1636"},{"id":"A693","pred":"tao:has_database_id","subj":"693","obj":"Gene:183"},{"id":"A694","pred":"tao:has_database_id","subj":"694","obj":"Gene:70008"},{"id":"A695","pred":"tao:has_database_id","subj":"695","obj":"Gene:70008"},{"id":"A696","pred":"tao:has_database_id","subj":"696","obj":"Gene:1636"},{"id":"A697","pred":"tao:has_database_id","subj":"697","obj":"Gene:70008"},{"id":"A698","pred":"tao:has_database_id","subj":"698","obj":"Tax:10090"},{"id":"A699","pred":"tao:has_database_id","subj":"699","obj":"Tax:10090"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}

{"project":"LitCovid-sentences","denotations":[{"id":"T165","span":{"begin":0,"end":264},"obj":"Sentence"},{"id":"T166","span":{"begin":265,"end":471},"obj":"Sentence"},{"id":"T167","span":{"begin":472,"end":698},"obj":"Sentence"},{"id":"T168","span":{"begin":699,"end":830},"obj":"Sentence"},{"id":"T169","span":{"begin":831,"end":966},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"After the initial discovery of ACE2 in the heart and kidney, it is now clear that it is widely distributed in tissues (section Tissue Distribution of ACE2), where it exerts many physiological effects and may be involved in pathophysiological events (Turner, 2015). The effect of ACE2 which has been more extensively investigated is the regulation of the RAAS system, where ACE2 counter-balances ACE, limiting the potent vasoconstrictive effect of angiotensin II (Ang-II). The first evidence that ACE2 was involved in RAAS control came from the transgenic knockout mouse model (ACE2–/–), which was characterized by severe reduction of cardiac contractility and thinning of the left ventricular wall. Interestingly, in this knockout model disruption of the ACE pathway could rescue the myocardial phenotype (Crackower et al., 2002). In another study, a selective ACE2 knockout model showed high blood pressure, worsened by the infusion of Ang-II (Gurley et al., 2006)."}