PMC:7565665 / 20842-21936 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T113","span":{"begin":133,"end":141},"obj":"Body_part"},{"id":"T114","span":{"begin":348,"end":350},"obj":"Body_part"},{"id":"T115","span":{"begin":411,"end":413},"obj":"Body_part"},{"id":"T116","span":{"begin":608,"end":612},"obj":"Body_part"},{"id":"T117","span":{"begin":630,"end":636},"obj":"Body_part"},{"id":"T118","span":{"begin":704,"end":708},"obj":"Body_part"}],"attributes":[{"id":"A113","pred":"fma_id","subj":"T113","obj":"http://purl.org/sig/ont/fma/fma264783"},{"id":"A114","pred":"fma_id","subj":"T114","obj":"http://purl.org/sig/ont/fma/fma284995"},{"id":"A115","pred":"fma_id","subj":"T115","obj":"http://purl.org/sig/ont/fma/fma284995"},{"id":"A116","pred":"fma_id","subj":"T116","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A117","pred":"fma_id","subj":"T117","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A118","pred":"fma_id","subj":"T118","obj":"http://purl.org/sig/ont/fma/fma7195"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T28","span":{"begin":608,"end":612},"obj":"Body_part"},{"id":"T29","span":{"begin":630,"end":636},"obj":"Body_part"},{"id":"T30","span":{"begin":704,"end":708},"obj":"Body_part"}],"attributes":[{"id":"A28","pred":"uberon_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A29","pred":"uberon_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A30","pred":"uberon_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T157","span":{"begin":188,"end":198},"obj":"Disease"},{"id":"T158","span":{"begin":281,"end":301},"obj":"Disease"},{"id":"T159","span":{"begin":622,"end":628},"obj":"Disease"},{"id":"T160","span":{"begin":704,"end":717},"obj":"Disease"},{"id":"T161","span":{"begin":727,"end":731},"obj":"Disease"},{"id":"T162","span":{"begin":732,"end":741},"obj":"Disease"},{"id":"T163","span":{"begin":760,"end":789},"obj":"Disease"},{"id":"T164","span":{"begin":771,"end":789},"obj":"Disease"},{"id":"T165","span":{"begin":791,"end":794},"obj":"Disease"}],"attributes":[{"id":"A157","pred":"mondo_id","subj":"T157","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A158","pred":"mondo_id","subj":"T158","obj":"http://purl.obolibrary.org/obo/MONDO_0005087"},{"id":"A159","pred":"mondo_id","subj":"T159","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A160","pred":"mondo_id","subj":"T160","obj":"http://purl.obolibrary.org/obo/MONDO_0005275"},{"id":"A161","pred":"mondo_id","subj":"T161","obj":"http://purl.obolibrary.org/obo/MONDO_0005002"},{"id":"A162","pred":"mondo_id","subj":"T162","obj":"http://purl.obolibrary.org/obo/MONDO_0004849"},{"id":"A163","pred":"mondo_id","subj":"T163","obj":"http://purl.obolibrary.org/obo/MONDO_0008345"},{"id":"A164","pred":"mondo_id","subj":"T164","obj":"http://purl.obolibrary.org/obo/MONDO_0002771"},{"id":"A165","pred":"mondo_id","subj":"T165","obj":"http://purl.obolibrary.org/obo/MONDO_0002429"},{"id":"A166","pred":"mondo_id","subj":"T165","obj":"http://purl.obolibrary.org/obo/MONDO_0008345"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T231","span":{"begin":0,"end":1},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T232","span":{"begin":452,"end":461},"obj":"http://www.ebi.ac.uk/efo/EFO_0000876"},{"id":"T233","span":{"begin":608,"end":612},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T234","span":{"begin":608,"end":612},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T235","span":{"begin":704,"end":708},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T236","span":{"begin":704,"end":708},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T85","span":{"begin":337,"end":340},"obj":"Chemical"},{"id":"T86","span":{"begin":348,"end":350},"obj":"Chemical"},{"id":"T87","span":{"begin":402,"end":405},"obj":"Chemical"},{"id":"T88","span":{"begin":411,"end":413},"obj":"Chemical"},{"id":"T89","span":{"begin":481,"end":484},"obj":"Chemical"},{"id":"T90","span":{"begin":527,"end":534},"obj":"Chemical"},{"id":"T91","span":{"begin":535,"end":546},"obj":"Chemical"},{"id":"T92","span":{"begin":899,"end":902},"obj":"Chemical"},{"id":"T93","span":{"begin":983,"end":994},"obj":"Chemical"},{"id":"T94","span":{"begin":995,"end":1000},"obj":"Chemical"}],"attributes":[{"id":"A85","pred":"chebi_id","subj":"T85","obj":"http://purl.obolibrary.org/obo/CHEBI_26523"},{"id":"A86","pred":"chebi_id","subj":"T86","obj":"http://purl.obolibrary.org/obo/CHEBI_73462"},{"id":"A87","pred":"chebi_id","subj":"T87","obj":"http://purl.obolibrary.org/obo/CHEBI_26523"},{"id":"A88","pred":"chebi_id","subj":"T88","obj":"http://purl.obolibrary.org/obo/CHEBI_73462"},{"id":"A89","pred":"chebi_id","subj":"T89","obj":"http://purl.obolibrary.org/obo/CHEBI_26523"},{"id":"A90","pred":"chebi_id","subj":"T90","obj":"http://purl.obolibrary.org/obo/CHEBI_63248"},{"id":"A91","pred":"chebi_id","subj":"T91","obj":"http://purl.obolibrary.org/obo/CHEBI_22586"},{"id":"A92","pred":"chebi_id","subj":"T92","obj":"http://purl.obolibrary.org/obo/CHEBI_26523"},{"id":"A93","pred":"chebi_id","subj":"T93","obj":"http://purl.obolibrary.org/obo/CHEBI_22586"},{"id":"A94","pred":"chebi_id","subj":"T94","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-PubTator","denotations":[{"id":"520","span":{"begin":348,"end":350},"obj":"Gene"},{"id":"521","span":{"begin":411,"end":413},"obj":"Gene"},{"id":"522","span":{"begin":337,"end":340},"obj":"Chemical"},{"id":"523","span":{"begin":402,"end":405},"obj":"Chemical"},{"id":"524","span":{"begin":481,"end":484},"obj":"Chemical"},{"id":"525","span":{"begin":899,"end":902},"obj":"Chemical"},{"id":"526","span":{"begin":188,"end":198},"obj":"Disease"},{"id":"527","span":{"begin":281,"end":301},"obj":"Disease"},{"id":"528","span":{"begin":608,"end":628},"obj":"Disease"},{"id":"529","span":{"begin":704,"end":717},"obj":"Disease"},{"id":"530","span":{"begin":727,"end":741},"obj":"Disease"},{"id":"531","span":{"begin":760,"end":789},"obj":"Disease"}],"attributes":[{"id":"A520","pred":"tao:has_database_id","subj":"520","obj":"Gene:1431"},{"id":"A521","pred":"tao:has_database_id","subj":"521","obj":"Gene:1431"},{"id":"A522","pred":"tao:has_database_id","subj":"522","obj":"MESH:D017382"},{"id":"A523","pred":"tao:has_database_id","subj":"523","obj":"MESH:D017382"},{"id":"A524","pred":"tao:has_database_id","subj":"524","obj":"MESH:D017382"},{"id":"A525","pred":"tao:has_database_id","subj":"525","obj":"MESH:D017382"},{"id":"A526","pred":"tao:has_database_id","subj":"526","obj":"MESH:D007239"},{"id":"A527","pred":"tao:has_database_id","subj":"527","obj":"MESH:D012140"},{"id":"A528","pred":"tao:has_database_id","subj":"528","obj":"MESH:D055370"},{"id":"A529","pred":"tao:has_database_id","subj":"529","obj":"MESH:D008171"},{"id":"A530","pred":"tao:has_database_id","subj":"530","obj":"MESH:D029424"},{"id":"A531","pred":"tao:has_database_id","subj":"531","obj":"MESH:D054990"}],"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":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T61","span":{"begin":115,"end":131},"obj":"Phenotype"},{"id":"T62","span":{"begin":178,"end":198},"obj":"Phenotype"},{"id":"T63","span":{"begin":692,"end":717},"obj":"Phenotype"},{"id":"T64","span":{"begin":727,"end":731},"obj":"Phenotype"},{"id":"T65","span":{"begin":732,"end":741},"obj":"Phenotype"},{"id":"T66","span":{"begin":771,"end":789},"obj":"Phenotype"}],"attributes":[{"id":"A61","pred":"hp_id","subj":"T61","obj":"http://purl.obolibrary.org/obo/HP_0025464"},{"id":"A62","pred":"hp_id","subj":"T62","obj":"http://purl.obolibrary.org/obo/HP_0002719"},{"id":"A63","pred":"hp_id","subj":"T63","obj":"http://purl.obolibrary.org/obo/HP_0002091"},{"id":"A64","pred":"hp_id","subj":"T64","obj":"http://purl.obolibrary.org/obo/HP_0006510"},{"id":"A65","pred":"hp_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/HP_0002097"},{"id":"A66","pred":"hp_id","subj":"T66","obj":"http://purl.obolibrary.org/obo/HP_0002206"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T295","span":{"begin":43,"end":52},"obj":"http://purl.obolibrary.org/obo/GO_0016236"},{"id":"T296","span":{"begin":43,"end":52},"obj":"http://purl.obolibrary.org/obo/GO_0006914"},{"id":"T297","span":{"begin":142,"end":151},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T298","span":{"begin":142,"end":151},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T299","span":{"begin":153,"end":172},"obj":"http://purl.obolibrary.org/obo/GO_0090398"},{"id":"T300","span":{"begin":231,"end":243},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T301","span":{"begin":653,"end":665},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T302","span":{"begin":941,"end":950},"obj":"http://purl.obolibrary.org/obo/GO_0016236"},{"id":"T303","span":{"begin":941,"end":950},"obj":"http://purl.obolibrary.org/obo/GO_0006914"},{"id":"T304","span":{"begin":1060,"end":1069},"obj":"http://purl.obolibrary.org/obo/GO_0016236"},{"id":"T305","span":{"begin":1060,"end":1069},"obj":"http://purl.obolibrary.org/obo/GO_0006914"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}

{"project":"LitCovid-sentences","denotations":[{"id":"T112","span":{"begin":0,"end":323},"obj":"Sentence"},{"id":"T113","span":{"begin":324,"end":568},"obj":"Sentence"},{"id":"T114","span":{"begin":569,"end":836},"obj":"Sentence"},{"id":"T115","span":{"begin":837,"end":1094},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. The inherent ROS in the CS, and the resulting increase in cellular endogenous ROS post-CS exposure, symbiotically contribute to extremely high intracellular ROS levels, which creates an imbalance in the oxidant–antioxidant ratio [22,34,61,112]. This serves as the basic mechanism for lung cellular injury, tissue damage, and the pathogenesis of chronic obstructive or restrictive lung diseases, such as COPD-emphysema (obstructive) and idiopathic pulmonary fibrosis (IPF, restrictive) [37,38,61,113,114,115,116]. Several groups including ours have demonstrated that elevated ROS levels are the key upstream driver of autophagy dysfunction, as treatments with antioxidant drugs rescues the age-related, or smoke, or eCV exposure-induced autophagy defect [15,22,42,61,62]."}