PMC:7799378 / 18683-19606 JSONTXT

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{"project":"LitCovid-sentences","denotations":[{"id":"T155","span":{"begin":0,"end":56},"obj":"Sentence"},{"id":"T156","span":{"begin":57,"end":253},"obj":"Sentence"},{"id":"T157","span":{"begin":254,"end":435},"obj":"Sentence"},{"id":"T158","span":{"begin":436,"end":584},"obj":"Sentence"},{"id":"T159","span":{"begin":585,"end":731},"obj":"Sentence"},{"id":"T160","span":{"begin":732,"end":923},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Elevated NET levels are found in COVID-19 patients [96]. NET formation is considered as a driver of COVID-19, since NET formation may contribute to tissue damage, organ injury, and mortality as indicated by autopsy specimens from COVID-19 patients [97]. The by-product of NETs, such as elastase, is involved in the pathogenesis of COVID-19 by facilitating SARS-CoV-2 entry and causing hypertension, thrombosis, and vasculitis [98–100]. The tissue damage leading to excessive oxidative stress creates a vicious cycle by increasing NET formation and distressing adaptive immunity [101]. Increased NETs are associated with hyperinflammation and in COVID-19 patients they amplify the severity and mortality associated with the disease. Targeting NETs and its feedback loop, with elastase, DNase-1, or inhibitory peptides as well as IL-1β, are potential therapeutic interventions for reducing the severity of COVID-19 [102,103]."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T32","span":{"begin":385,"end":397},"obj":"Phenotype"},{"id":"T33","span":{"begin":415,"end":425},"obj":"Phenotype"},{"id":"T34","span":{"begin":475,"end":491},"obj":"Phenotype"}],"attributes":[{"id":"A32","pred":"hp_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/HP_0000822"},{"id":"A33","pred":"hp_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/HP_0002633"},{"id":"A34","pred":"hp_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/HP_0025464"}],"text":"Elevated NET levels are found in COVID-19 patients [96]. NET formation is considered as a driver of COVID-19, since NET formation may contribute to tissue damage, organ injury, and mortality as indicated by autopsy specimens from COVID-19 patients [97]. The by-product of NETs, such as elastase, is involved in the pathogenesis of COVID-19 by facilitating SARS-CoV-2 entry and causing hypertension, thrombosis, and vasculitis [98–100]. The tissue damage leading to excessive oxidative stress creates a vicious cycle by increasing NET formation and distressing adaptive immunity [101]. Increased NETs are associated with hyperinflammation and in COVID-19 patients they amplify the severity and mortality associated with the disease. Targeting NETs and its feedback loop, with elastase, DNase-1, or inhibitory peptides as well as IL-1β, are potential therapeutic interventions for reducing the severity of COVID-19 [102,103]."}