PMC:7546716 / 1054-1333 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T20","span":{"begin":64,"end":66},"obj":"Body_part"},{"id":"T21","span":{"begin":113,"end":127},"obj":"Body_part"}],"attributes":[{"id":"A20","pred":"fma_id","subj":"T20","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A21","pred":"fma_id","subj":"T21","obj":"http://purl.org/sig/ont/fma/fma0326458"}],"text":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T8","span":{"begin":11,"end":21},"obj":"Disease"},{"id":"T9","span":{"begin":54,"end":62},"obj":"Disease"},{"id":"T10","span":{"begin":82,"end":100},"obj":"Disease"}],"attributes":[{"id":"A8","pred":"mondo_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/MONDO_0000831"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/MONDO_0002771"}],"text":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T11","span":{"begin":132,"end":142},"obj":"http://purl.obolibrary.org/obo/CL_0000066"}],"text":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T11","span":{"begin":64,"end":66},"obj":"Chemical"}],"attributes":[{"id":"A11","pred":"chebi_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A12","pred":"chebi_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"}],"text":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T2","span":{"begin":82,"end":100},"obj":"Phenotype"}],"attributes":[{"id":"A2","pred":"hp_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/HP_0002206"}],"text":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T1","span":{"begin":132,"end":165},"obj":"http://purl.obolibrary.org/obo/GO_0001837"}],"text":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}

{"project":"LitCovid-sentences","denotations":[{"id":"T8","span":{"begin":23,"end":166},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}

{"project":"LitCovid-PubTator","denotations":[{"id":"29","span":{"begin":64,"end":69},"obj":"Gene"},{"id":"34","span":{"begin":26,"end":34},"obj":"Species"},{"id":"40","span":{"begin":54,"end":62},"obj":"Disease"},{"id":"41","span":{"begin":82,"end":100},"obj":"Disease"}],"attributes":[{"id":"A29","pred":"tao:has_database_id","subj":"29","obj":"Gene:90865"},{"id":"A34","pred":"tao:has_database_id","subj":"34","obj":"Tax:9606"},{"id":"A40","pred":"tao:has_database_id","subj":"40","obj":"MESH:C000657245"},{"id":"A41","pred":"tao:has_database_id","subj":"41","obj":"MESH:D011658"}],"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":"and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target I"}