PMC:7170368 / 9958-11712 JSON TXT

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LitCovid-PubTator

MyTest

{"project":"MyTest","denotations":[{"id":"32228222-31838905-27780685","span":{"begin":303,"end":304},"obj":"31838905"},{"id":"32228222-31805278-27780686","span":{"begin":992,"end":994},"obj":"31805278"},{"id":"32228222-15067208-27780687","span":{"begin":1167,"end":1169},"obj":"15067208"}],"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":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T27","span":{"begin":180,"end":184},"obj":"Body_part"},{"id":"T28","span":{"begin":374,"end":383},"obj":"Body_part"},{"id":"T29","span":{"begin":461,"end":470},"obj":"Body_part"},{"id":"T30","span":{"begin":1023,"end":1028},"obj":"Body_part"},{"id":"T31","span":{"begin":1113,"end":1121},"obj":"Body_part"},{"id":"T32","span":{"begin":1146,"end":1154},"obj":"Body_part"},{"id":"T33","span":{"begin":1250,"end":1263},"obj":"Body_part"},{"id":"T34","span":{"begin":1289,"end":1293},"obj":"Body_part"},{"id":"T35","span":{"begin":1382,"end":1386},"obj":"Body_part"}],"attributes":[{"id":"A27","pred":"fma_id","subj":"T27","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A28","pred":"fma_id","subj":"T28","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A29","pred":"fma_id","subj":"T29","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A30","pred":"fma_id","subj":"T30","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A31","pred":"fma_id","subj":"T31","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A32","pred":"fma_id","subj":"T32","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A33","pred":"fma_id","subj":"T33","obj":"http://purl.org/sig/ont/fma/fma9825"},{"id":"A34","pred":"fma_id","subj":"T34","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A35","pred":"fma_id","subj":"T35","obj":"http://purl.org/sig/ont/fma/fma7195"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T27","span":{"begin":180,"end":184},"obj":"Body_part"},{"id":"T28","span":{"begin":207,"end":210},"obj":"Body_part"},{"id":"T29","span":{"begin":621,"end":624},"obj":"Body_part"},{"id":"T30","span":{"begin":1023,"end":1028},"obj":"Body_part"},{"id":"T31","span":{"begin":1250,"end":1263},"obj":"Body_part"},{"id":"T32","span":{"begin":1382,"end":1386},"obj":"Body_part"},{"id":"T33","span":{"begin":1492,"end":1495},"obj":"Body_part"}],"attributes":[{"id":"A27","pred":"uberon_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A28","pred":"uberon_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"},{"id":"A29","pred":"uberon_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"},{"id":"A30","pred":"uberon_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A31","pred":"uberon_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/UBERON_0002405"},{"id":"A32","pred":"uberon_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A33","pred":"uberon_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T88","span":{"begin":28,"end":36},"obj":"Disease"},{"id":"T89","span":{"begin":163,"end":175},"obj":"Disease"},{"id":"T90","span":{"begin":502,"end":510},"obj":"Disease"},{"id":"T91","span":{"begin":570,"end":578},"obj":"Disease"},{"id":"T92","span":{"begin":712,"end":720},"obj":"Disease"},{"id":"T93","span":{"begin":735,"end":747},"obj":"Disease"},{"id":"T94","span":{"begin":786,"end":789},"obj":"Disease"},{"id":"T95","span":{"begin":939,"end":942},"obj":"Disease"},{"id":"T96","span":{"begin":984,"end":990},"obj":"Disease"},{"id":"T97","span":{"begin":1023,"end":1036},"obj":"Disease"},{"id":"T98","span":{"begin":1207,"end":1210},"obj":"Disease"},{"id":"T99","span":{"begin":1387,"end":1393},"obj":"Disease"},{"id":"T100","span":{"begin":1430,"end":1433},"obj":"Disease"}],"attributes":[{"id":"A88","pred":"mondo_id","subj":"T88","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A89","pred":"mondo_id","subj":"T89","obj":"http://purl.obolibrary.org/obo/MONDO_0005044"},{"id":"A90","pred":"mondo_id","subj":"T90","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A91","pred":"mondo_id","subj":"T91","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A92","pred":"mondo_id","subj":"T92","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A93","pred":"mondo_id","subj":"T93","obj":"http://purl.obolibrary.org/obo/MONDO_0005044"},{"id":"A94","pred":"mondo_id","subj":"T94","obj":"http://purl.obolibrary.org/obo/MONDO_0012733"},{"id":"A95","pred":"mondo_id","subj":"T95","obj":"http://purl.obolibrary.org/obo/MONDO_0012733"},{"id":"A96","pred":"mondo_id","subj":"T96","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A97","pred":"mondo_id","subj":"T97","obj":"http://purl.obolibrary.org/obo/MONDO_0005252"},{"id":"A98","pred":"mondo_id","subj":"T98","obj":"http://purl.obolibrary.org/obo/MONDO_0012733"},{"id":"A99","pred":"mondo_id","subj":"T99","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A100","pred":"mondo_id","subj":"T100","obj":"http://purl.obolibrary.org/obo/MONDO_0012733"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T86","span":{"begin":180,"end":184},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T87","span":{"begin":180,"end":184},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T88","span":{"begin":396,"end":406},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T89","span":{"begin":677,"end":680},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T90","span":{"begin":992,"end":994},"obj":"http://purl.obolibrary.org/obo/CLO_0053733"},{"id":"T91","span":{"begin":1023,"end":1028},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T92","span":{"begin":1023,"end":1028},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T93","span":{"begin":1023,"end":1028},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T94","span":{"begin":1023,"end":1028},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T95","span":{"begin":1041,"end":1044},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T96","span":{"begin":1223,"end":1224},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T97","span":{"begin":1250,"end":1263},"obj":"http://purl.obolibrary.org/obo/UBERON_0002405"},{"id":"T98","span":{"begin":1287,"end":1293},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T99","span":{"begin":1382,"end":1386},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T100","span":{"begin":1382,"end":1386},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

LitCovid-PD-CHEBI

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T2","span":{"begin":813,"end":834},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T3","span":{"begin":1146,"end":1165},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T4","span":{"begin":1523,"end":1548},"obj":"http://purl.obolibrary.org/obo/GO_1903901"},{"id":"T5","span":{"begin":1531,"end":1548},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T6","span":{"begin":1531,"end":1548},"obj":"http://purl.obolibrary.org/obo/GO_0019058"},{"id":"T7","span":{"begin":1629,"end":1671},"obj":"http://purl.obolibrary.org/obo/GO_0050728"},{"id":"T8","span":{"begin":1640,"end":1662},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T84","span":{"begin":0,"end":107},"obj":"Sentence"},{"id":"T85","span":{"begin":108,"end":193},"obj":"Sentence"},{"id":"T86","span":{"begin":194,"end":306},"obj":"Sentence"},{"id":"T87","span":{"begin":307,"end":420},"obj":"Sentence"},{"id":"T88","span":{"begin":421,"end":520},"obj":"Sentence"},{"id":"T89","span":{"begin":521,"end":625},"obj":"Sentence"},{"id":"T90","span":{"begin":626,"end":696},"obj":"Sentence"},{"id":"T91","span":{"begin":697,"end":996},"obj":"Sentence"},{"id":"T92","span":{"begin":997,"end":1171},"obj":"Sentence"},{"id":"T93","span":{"begin":1172,"end":1304},"obj":"Sentence"},{"id":"T94","span":{"begin":1305,"end":1398},"obj":"Sentence"},{"id":"T95","span":{"begin":1399,"end":1754},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T24","span":{"begin":163,"end":175},"obj":"Phenotype"},{"id":"T25","span":{"begin":295,"end":301},"obj":"Phenotype"},{"id":"T26","span":{"begin":735,"end":747},"obj":"Phenotype"},{"id":"T27","span":{"begin":1015,"end":1036},"obj":"Phenotype"}],"attributes":[{"id":"A24","pred":"hp_id","subj":"T24","obj":"http://purl.obolibrary.org/obo/HP_0000822"},{"id":"A25","pred":"hp_id","subj":"T25","obj":"http://purl.obolibrary.org/obo/HP_0100806"},{"id":"A26","pred":"hp_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/HP_0000822"},{"id":"A27","pred":"hp_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/HP_0001635"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

2_test

{"project":"2_test","denotations":[{"id":"32228222-31838905-27780685","span":{"begin":303,"end":304},"obj":"31838905"},{"id":"32228222-31805278-27780686","span":{"begin":992,"end":994},"obj":"31805278"},{"id":"32228222-15067208-27780687","span":{"begin":1167,"end":1169},"obj":"15067208"}],"text":"Studies have suggested that COVID-19 patients have increased Angiotensin II compared to healthy people [8]. The abnormal increase in Angiotensin II was related to hypertension and lung failure. In addition, RAS inhibitors have been shown to be associated with reduced mortality in patients with sepsis [9]. Angiotensin II positively regulates the expression of inflammatory cytokines through the activation of AT1R [10]. Excessively high levels of inflammatory cytokines are harmful to the outcomes of COVID-19 patients. Thus, it was suggested that it is beneficial for COVID-19 patients to use ACEIs/ARBs to inhibit the RAS. However, until now, no confirmed clinical evidence has been available. In this study, COVID-19 patients with hypertension were enrolled, and we found that ACEI/ARB therapy attenuated the inflammatory response, potentially through the inhibition of IL-6 levels, which is consistent with the findings that ACEI and ARB therapy alleviated LPS-induced pneumonic injury [11]. For patients with chronic heart failure, it has been proven that ACEI therapy was associated with decreased Th1/Th2 cytokine ratios and inflammatory cytokine production [12]. This study also suggests that ACEI/ARB therapy had a beneficial effect on the immune system by avoiding peripheral T cell depletion. Furthermore, the viral load was reported to be highly correlated with severe lung injury [8]. It was also observed that ACEI/ARB therapy decreased the viral load, but we hypothesize that RAS inhibitors do not directly inhibit viral replication; rather, they play an indirect antiviral role by regulating immune function and inhibiting inflammatory responses, and the mechanism needs to be clarified through in vitro and in vivostudies in the future."}

PMC:7170368 / 9958-11712 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7170368 / 9958-11712 JSON TXT