PMC:7335494 / 3344-4873 JSON TXT

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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T9","span":{"begin":92,"end":98},"obj":"Body_part"},{"id":"T10","span":{"begin":157,"end":163},"obj":"Body_part"},{"id":"T11","span":{"begin":828,"end":835},"obj":"Body_part"},{"id":"T12","span":{"begin":1072,"end":1081},"obj":"Body_part"},{"id":"T13","span":{"begin":1109,"end":1121},"obj":"Body_part"},{"id":"T14","span":{"begin":1123,"end":1127},"obj":"Body_part"},{"id":"T15","span":{"begin":1180,"end":1203},"obj":"Body_part"},{"id":"T16","span":{"begin":1180,"end":1184},"obj":"Body_part"},{"id":"T17","span":{"begin":1208,"end":1218},"obj":"Body_part"}],"attributes":[{"id":"A9","pred":"fma_id","subj":"T9","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A10","pred":"fma_id","subj":"T10","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A11","pred":"fma_id","subj":"T11","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A12","pred":"fma_id","subj":"T12","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A13","pred":"fma_id","subj":"T13","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A14","pred":"fma_id","subj":"T14","obj":"http://purl.org/sig/ont/fma/fma86583"},{"id":"A15","pred":"fma_id","subj":"T15","obj":"http://purl.org/sig/ont/fma/fma67214"},{"id":"A16","pred":"fma_id","subj":"T16","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A17","pred":"fma_id","subj":"T17","obj":"http://purl.org/sig/ont/fma/fma241981"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T5","span":{"begin":92,"end":98},"obj":"Body_part"},{"id":"T6","span":{"begin":157,"end":163},"obj":"Body_part"}],"attributes":[{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T26","span":{"begin":32,"end":44},"obj":"Disease"},{"id":"T27","span":{"begin":320,"end":332},"obj":"Disease"},{"id":"T28","span":{"begin":549,"end":561},"obj":"Disease"}],"attributes":[{"id":"A26","pred":"mondo_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A27","pred":"mondo_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A28","pred":"mondo_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T16","span":{"begin":48,"end":49},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T17","span":{"begin":109,"end":110},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T18","span":{"begin":701,"end":702},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T19","span":{"begin":786,"end":787},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T20","span":{"begin":849,"end":850},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T21","span":{"begin":944,"end":950},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T22","span":{"begin":966,"end":975},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T23","span":{"begin":1061,"end":1062},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T24","span":{"begin":1068,"end":1069},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T25","span":{"begin":1135,"end":1139},"obj":"http://purl.obolibrary.org/obo/CLO_0053704"},{"id":"T26","span":{"begin":1180,"end":1184},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

LitCovid-PD-CHEBI

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T6","span":{"begin":32,"end":44},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T7","span":{"begin":157,"end":175},"obj":"http://purl.obolibrary.org/obo/GO_0001894"},{"id":"T8","span":{"begin":164,"end":175},"obj":"http://purl.obolibrary.org/obo/GO_0042592"},{"id":"T9","span":{"begin":195,"end":217},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T10","span":{"begin":320,"end":332},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T11","span":{"begin":549,"end":561},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T12","span":{"begin":979,"end":992},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T13","span":{"begin":1149,"end":1157},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T14","span":{"begin":1149,"end":1157},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T15","span":{"begin":1149,"end":1157},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T16","span":{"begin":1149,"end":1157},"obj":"http://purl.obolibrary.org/obo/GO_0001906"},{"id":"T17","span":{"begin":1180,"end":1203},"obj":"http://purl.obolibrary.org/obo/GO_0098631"},{"id":"T18","span":{"begin":1180,"end":1193},"obj":"http://purl.obolibrary.org/obo/GO_0007155"},{"id":"T19","span":{"begin":1326,"end":1335},"obj":"http://purl.obolibrary.org/obo/GO_0009058"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T21","span":{"begin":0,"end":194},"obj":"Sentence"},{"id":"T22","span":{"begin":195,"end":381},"obj":"Sentence"},{"id":"T23","span":{"begin":382,"end":630},"obj":"Sentence"},{"id":"T24","span":{"begin":631,"end":836},"obj":"Sentence"},{"id":"T25","span":{"begin":837,"end":1224},"obj":"Sentence"},{"id":"T26","span":{"begin":1225,"end":1529},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T12","span":{"begin":1142,"end":1148},"obj":"Phenotype"}],"attributes":[{"id":"A12","pred":"hp_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/HP_0002664"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

MyTest

{"project":"MyTest","denotations":[{"id":"32640331-18650913-30720712","span":{"begin":188,"end":192},"obj":"18650913"},{"id":"32640331-26688348-30720713","span":{"begin":350,"end":354},"obj":"26688348"},{"id":"32640331-16369558-30720714","span":{"begin":375,"end":379},"obj":"16369558"},{"id":"32640331-20497301-30720715","span":{"begin":596,"end":600},"obj":"20497301"},{"id":"32640331-24400794-30720716","span":{"begin":624,"end":628},"obj":"24400794"},{"id":"32640331-26228057-30720717","span":{"begin":1475,"end":1479},"obj":"26228057"},{"id":"32640331-23592557-30720718","span":{"begin":1502,"end":1506},"obj":"23592557"},{"id":"32640331-18437155-30720719","span":{"begin":1523,"end":1527},"obj":"18437155"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

2_test

{"project":"2_test","denotations":[{"id":"32640331-18650913-30720712","span":{"begin":188,"end":192},"obj":"18650913"},{"id":"32640331-26688348-30720713","span":{"begin":350,"end":354},"obj":"26688348"},{"id":"32640331-16369558-30720714","span":{"begin":375,"end":379},"obj":"16369558"},{"id":"32640331-20497301-30720715","span":{"begin":596,"end":600},"obj":"20497301"},{"id":"32640331-24400794-30720716","span":{"begin":624,"end":628},"obj":"24400794"},{"id":"32640331-26228057-30720717","span":{"begin":1475,"end":1479},"obj":"26228057"},{"id":"32640331-23592557-30720718","span":{"begin":1502,"end":1506},"obj":"23592557"},{"id":"32640331-18437155-30720719","span":{"begin":1523,"end":1527},"obj":"18437155"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

LitCovid-PMC-OGER-BB

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T37","span":{"begin":92,"end":98},"obj":"UBERON:0000479"},{"id":"T38","span":{"begin":111,"end":128},"obj":"GO:0051866"},{"id":"T39","span":{"begin":157,"end":163},"obj":"UBERON:0000479;GO:0001894"},{"id":"T40","span":{"begin":164,"end":175},"obj":"GO:0001894"},{"id":"T41","span":{"begin":208,"end":217},"obj":"GO:0002437"},{"id":"T42","span":{"begin":252,"end":263},"obj":"GO:0000075"},{"id":"T43","span":{"begin":492,"end":508},"obj":"CHEBI:67079;CHEBI:67079"},{"id":"T44","span":{"begin":509,"end":518},"obj":"CHEBI:36357;CHEBI:36357"},{"id":"T45","span":{"begin":674,"end":681},"obj":"GO:0006952"},{"id":"T46","span":{"begin":750,"end":758},"obj":"CHEBI:75958;CHEBI:75958"},{"id":"T47","span":{"begin":828,"end":835},"obj":"UBERON:0000479"},{"id":"T48","span":{"begin":865,"end":878},"obj":"GO:0065007"},{"id":"T49","span":{"begin":918,"end":934},"obj":"PR:000013428"},{"id":"T50","span":{"begin":936,"end":941},"obj":"PR:000013428"},{"id":"T51","span":{"begin":944,"end":994},"obj":"PR:000002089"},{"id":"T52","span":{"begin":996,"end":1001},"obj":"PR:000002089"},{"id":"T53","span":{"begin":1004,"end":1010},"obj":"GO:0031012;PR:000010491"},{"id":"T54","span":{"begin":1011,"end":1030},"obj":"PR:000010491"},{"id":"T55","span":{"begin":1032,"end":1037},"obj":"PR:000010491"},{"id":"T56","span":{"begin":1064,"end":1066},"obj":"GO:0005883"},{"id":"T57","span":{"begin":1129,"end":1133},"obj":"PR:000001393"},{"id":"T58","span":{"begin":1135,"end":1139},"obj":"PR:000001395"},{"id":"T59","span":{"begin":1172,"end":1177},"obj":"PR:000000134"},{"id":"T60","span":{"begin":1194,"end":1203},"obj":"CHEBI:36357;CHEBI:36357"},{"id":"T61","span":{"begin":1346,"end":1359},"obj":"CHEBI:67079;CHEBI:67079"},{"id":"T62","span":{"begin":1360,"end":1369},"obj":"CHEBI:36357;CHEBI:36357"},{"id":"T63","span":{"begin":1416,"end":1428},"obj":"CHEBI:67079;CHEBI:67079"},{"id":"T64","span":{"begin":1447,"end":1456},"obj":"CHEBI:36357;CHEBI:36357"}],"text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008)."}

PMC:7335494 / 3344-4873 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7335494 / 3344-4873 JSON TXT