PMC:7283670 / 125274-126251 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T92","span":{"begin":31,"end":34},"obj":"Body_part"},{"id":"T93","span":{"begin":47,"end":51},"obj":"Body_part"},{"id":"T94","span":{"begin":261,"end":267},"obj":"Body_part"},{"id":"T95","span":{"begin":941,"end":947},"obj":"Body_part"}],"attributes":[{"id":"A92","pred":"fma_id","subj":"T92","obj":"http://purl.org/sig/ont/fma/fma24890"},{"id":"A93","pred":"fma_id","subj":"T93","obj":"http://purl.org/sig/ont/fma/fma12520"},{"id":"A94","pred":"fma_id","subj":"T94","obj":"http://purl.org/sig/ont/fma/fma62970"},{"id":"A95","pred":"fma_id","subj":"T95","obj":"http://purl.org/sig/ont/fma/fma9637"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T234","span":{"begin":31,"end":34},"obj":"Body_part"},{"id":"T235","span":{"begin":941,"end":947},"obj":"Body_part"}],"attributes":[{"id":"A234","pred":"uberon_id","subj":"T234","obj":"http://purl.obolibrary.org/obo/UBERON_0001460"},{"id":"A235","pred":"uberon_id","subj":"T235","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T681","span":{"begin":201,"end":213},"obj":"Disease"},{"id":"T682","span":{"begin":317,"end":326},"obj":"Disease"},{"id":"T683","span":{"begin":433,"end":442},"obj":"Disease"},{"id":"T684","span":{"begin":447,"end":472},"obj":"Disease"},{"id":"T686","span":{"begin":494,"end":498},"obj":"Disease"},{"id":"T687","span":{"begin":754,"end":762},"obj":"Disease"}],"attributes":[{"id":"A681","pred":"mondo_id","subj":"T681","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A682","pred":"mondo_id","subj":"T682","obj":"http://purl.obolibrary.org/obo/MONDO_0005249"},{"id":"A683","pred":"mondo_id","subj":"T683","obj":"http://purl.obolibrary.org/obo/MONDO_0005249"},{"id":"A684","pred":"mondo_id","subj":"T684","obj":"http://purl.obolibrary.org/obo/MONDO_0001208"},{"id":"A685","pred":"mondo_id","subj":"T684","obj":"http://purl.obolibrary.org/obo/MONDO_0021113"},{"id":"A686","pred":"mondo_id","subj":"T686","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A687","pred":"mondo_id","subj":"T687","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T172","span":{"begin":8,"end":9},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T173","span":{"begin":31,"end":34},"obj":"http://www.ebi.ac.uk/efo/EFO_0001410"},{"id":"T174","span":{"begin":59,"end":60},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T175","span":{"begin":261,"end":267},"obj":"http://purl.obolibrary.org/obo/UBERON_0001969"},{"id":"T176","span":{"begin":347,"end":353},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_33208"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T265","span":{"begin":79,"end":93},"obj":"Chemical"},{"id":"T266","span":{"begin":91,"end":93},"obj":"Chemical"},{"id":"T267","span":{"begin":94,"end":105},"obj":"Chemical"},{"id":"T2111","span":{"begin":139,"end":150},"obj":"Chemical"},{"id":"T13587","span":{"begin":243,"end":257},"obj":"Chemical"},{"id":"T82878","span":{"begin":255,"end":257},"obj":"Chemical"},{"id":"T77587","span":{"begin":397,"end":407},"obj":"Chemical"},{"id":"T42101","span":{"begin":588,"end":599},"obj":"Chemical"},{"id":"T86413","span":{"begin":673,"end":683},"obj":"Chemical"}],"attributes":[{"id":"A99410","pred":"chebi_id","subj":"T265","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A58585","pred":"chebi_id","subj":"T266","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A4493","pred":"chebi_id","subj":"T267","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A6603","pred":"chebi_id","subj":"T2111","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A34415","pred":"chebi_id","subj":"T13587","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A24342","pred":"chebi_id","subj":"T82878","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A56157","pred":"chebi_id","subj":"T77587","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A35511","pred":"chebi_id","subj":"T42101","obj":"http://purl.obolibrary.org/obo/CHEBI_2719"},{"id":"A43180","pred":"chebi_id","subj":"T86413","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T19","span":{"begin":201,"end":213},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T20","span":{"begin":810,"end":821},"obj":"http://purl.obolibrary.org/obo/GO_0042592"},{"id":"T21","span":{"begin":838,"end":849},"obj":"http://purl.obolibrary.org/obo/GO_0042592"},{"id":"T22","span":{"begin":894,"end":915},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-sentences","denotations":[{"id":"T1039","span":{"begin":0,"end":214},"obj":"Sentence"},{"id":"T1040","span":{"begin":215,"end":327},"obj":"Sentence"},{"id":"T1041","span":{"begin":328,"end":473},"obj":"Sentence"},{"id":"T1042","span":{"begin":474,"end":627},"obj":"Sentence"},{"id":"T1043","span":{"begin":628,"end":822},"obj":"Sentence"},{"id":"T1044","span":{"begin":823,"end":977},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T320","span":{"begin":317,"end":326},"obj":"Phenotype"},{"id":"T321","span":{"begin":433,"end":442},"obj":"Phenotype"},{"id":"T322","span":{"begin":453,"end":472},"obj":"Phenotype"}],"attributes":[{"id":"A320","pred":"hp_id","subj":"T320","obj":"http://purl.obolibrary.org/obo/HP_0002090"},{"id":"A321","pred":"hp_id","subj":"T321","obj":"http://purl.obolibrary.org/obo/HP_0002090"},{"id":"A322","pred":"hp_id","subj":"T322","obj":"http://purl.obolibrary.org/obo/HP_0002878"}],"text":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}

{"project":"LitCovid-PubTator","denotations":[{"id":"2592","span":{"begin":0,"end":4},"obj":"Gene"},{"id":"2593","span":{"begin":75,"end":78},"obj":"Gene"},{"id":"2594","span":{"begin":123,"end":127},"obj":"Gene"},{"id":"2595","span":{"begin":134,"end":138},"obj":"Gene"},{"id":"2596","span":{"begin":235,"end":238},"obj":"Gene"},{"id":"2597","span":{"begin":243,"end":257},"obj":"Gene"},{"id":"2598","span":{"begin":509,"end":513},"obj":"Gene"},{"id":"2599","span":{"begin":583,"end":587},"obj":"Gene"},{"id":"2600","span":{"begin":660,"end":663},"obj":"Gene"},{"id":"2601","span":{"begin":668,"end":672},"obj":"Gene"},{"id":"2602","span":{"begin":494,"end":504},"obj":"Species"},{"id":"2603","span":{"begin":763,"end":771},"obj":"Species"},{"id":"2604","span":{"begin":201,"end":213},"obj":"Disease"},{"id":"2605","span":{"begin":317,"end":326},"obj":"Disease"},{"id":"2606","span":{"begin":433,"end":442},"obj":"Disease"},{"id":"2607","span":{"begin":453,"end":472},"obj":"Disease"},{"id":"2608","span":{"begin":754,"end":762},"obj":"Disease"},{"id":"2609","span":{"begin":789,"end":800},"obj":"Disease"}],"attributes":[{"id":"A2592","pred":"tao:has_database_id","subj":"2592","obj":"Gene:59272"},{"id":"A2593","pred":"tao:has_database_id","subj":"2593","obj":"Gene:1636"},{"id":"A2594","pred":"tao:has_database_id","subj":"2594","obj":"Gene:185"},{"id":"A2595","pred":"tao:has_database_id","subj":"2595","obj":"Gene:59272"},{"id":"A2596","pred":"tao:has_database_id","subj":"2596","obj":"Gene:1636"},{"id":"A2597","pred":"tao:has_database_id","subj":"2597","obj":"Gene:183"},{"id":"A2598","pred":"tao:has_database_id","subj":"2598","obj":"Gene:59272"},{"id":"A2599","pred":"tao:has_database_id","subj":"2599","obj":"Gene:59272"},{"id":"A2600","pred":"tao:has_database_id","subj":"2600","obj":"Gene:1636"},{"id":"A2601","pred":"tao:has_database_id","subj":"2601","obj":"Gene:185"},{"id":"A2602","pred":"tao:has_database_id","subj":"2602","obj":"Tax:2697049"},{"id":"A2603","pred":"tao:has_database_id","subj":"2603","obj":"Tax:9606"},{"id":"A2604","pred":"tao:has_database_id","subj":"2604","obj":"MESH:D007249"},{"id":"A2605","pred":"tao:has_database_id","subj":"2605","obj":"MESH:D011014"},{"id":"A2606","pred":"tao:has_database_id","subj":"2606","obj":"MESH:D011014"},{"id":"A2607","pred":"tao:has_database_id","subj":"2607","obj":"MESH:D012131"},{"id":"A2608","pred":"tao:has_database_id","subj":"2608","obj":"MESH:C000657245"},{"id":"A2609","pred":"tao:has_database_id","subj":"2609","obj":"MESH:D060825"}],"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":"ACE2 is a prominent regulatory arm in the RAAS axis, thus, a disruption in ACE‐Angiotensin II‐Angiotensin Type 1 Receptor (AT1R), and ACE2/Angiotensin‐(1‐7)/Mas Receptor axes can result in multisystem inflammation. Increased levels of ACE and Angiotensin II in plasma are considered poor prognostic factors in severe pneumonia. Several studies on animal models have reported effectiveness of RAAS inhibitors in alleviation of severe pneumonia and acute respiratory failure. In the aftermath of SARS‐CoV‐2 and ACE2 binding, the enzyme is eventually degraded, hence, the inhibition of ACE2/Angiotensin‐(1‐7)/Mas Receptor pathway. Accordingly, it is assumed that ACE and AT1R inhibitors might be game‐changing agents that can especially be administered for COVID‐19 patients who have serious impairments in their homeostasis. Maintenance of homeostasis may ultimately result in suppression of the inflammatory response, mostly in the pulmonary tissue (Sun, Yang, Sun, \u0026 Su, 2020)."}