PMC:7161517 / 8808-9732 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T52","span":{"begin":356,"end":371},"obj":"Body_part"},{"id":"T53","span":{"begin":376,"end":396},"obj":"Body_part"},{"id":"T54","span":{"begin":406,"end":425},"obj":"Body_part"}],"attributes":[{"id":"A52","pred":"fma_id","subj":"T52","obj":"http://purl.org/sig/ont/fma/fma15633"},{"id":"A53","pred":"fma_id","subj":"T53","obj":"http://purl.org/sig/ont/fma/fma74646"},{"id":"A54","pred":"fma_id","subj":"T54","obj":"http://purl.org/sig/ont/fma/fma74636"}],"text":"Angiotensinogen is converted to angiotensin I (Ang I) via renin. Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). RAS = renin-angiotensin system."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T32","span":{"begin":356,"end":371},"obj":"Body_part"},{"id":"T33","span":{"begin":893,"end":896},"obj":"Body_part"},{"id":"T34","span":{"begin":899,"end":923},"obj":"Body_part"}],"attributes":[{"id":"A32","pred":"uberon_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/UBERON_0001236"},{"id":"A33","pred":"uberon_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"},{"id":"A34","pred":"uberon_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/UBERON_0018229"}],"text":"Angiotensinogen is converted to angiotensin I (Ang I) via renin. Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). RAS = renin-angiotensin system."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T47","span":{"begin":209,"end":221},"obj":"Disease"},{"id":"T48","span":{"begin":302,"end":305},"obj":"Disease"},{"id":"T49","span":{"begin":416,"end":425},"obj":"Disease"}],"attributes":[{"id":"A47","pred":"mondo_id","subj":"T47","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A48","pred":"mondo_id","subj":"T48","obj":"http://purl.obolibrary.org/obo/MONDO_0008840"},{"id":"A49","pred":"mondo_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/MONDO_0021156"}],"text":"Angiotensinogen is converted to angiotensin I (Ang I) via renin. Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). RAS = renin-angiotensin system."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T102","span":{"begin":406,"end":415},"obj":"http://purl.obolibrary.org/obo/UBERON_0001353"},{"id":"T103","span":{"begin":449,"end":457},"obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"T104","span":{"begin":540,"end":546},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T105","span":{"begin":854,"end":864},"obj":"http://purl.obolibrary.org/obo/PR_000001898"}],"text":"Angiotensinogen is converted to angiotensin I (Ang I) via renin. Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). RAS = renin-angiotensin system."}

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{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T31","span":{"begin":209,"end":221},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T32","span":{"begin":325,"end":346},"obj":"http://purl.obolibrary.org/obo/GO_0035932"},{"id":"T33","span":{"begin":337,"end":346},"obj":"http://purl.obolibrary.org/obo/GO_0046903"},{"id":"T34","span":{"begin":564,"end":570},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T35","span":{"begin":571,"end":575},"obj":"http://purl.obolibrary.org/obo/GO_0004707"}],"text":"Angiotensinogen is converted to angiotensin I (Ang I) via renin. Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). RAS = renin-angiotensin system."}

{"project":"LitCovid-sentences","denotations":[{"id":"T59","span":{"begin":0,"end":64},"obj":"Sentence"},{"id":"T60","span":{"begin":65,"end":222},"obj":"Sentence"},{"id":"T61","span":{"begin":223,"end":426},"obj":"Sentence"},{"id":"T62","span":{"begin":427,"end":474},"obj":"Sentence"},{"id":"T63","span":{"begin":475,"end":585},"obj":"Sentence"},{"id":"T64","span":{"begin":586,"end":739},"obj":"Sentence"},{"id":"T65","span":{"begin":740,"end":892},"obj":"Sentence"},{"id":"T66","span":{"begin":893,"end":924},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Angiotensinogen is converted to angiotensin I (Ang I) via renin. Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). RAS = renin-angiotensin system."}

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Ang I is converted to Ang II via angiotensin-converting enzyme (ACE), which also hydrolyzes bradykinin into its inactive metabolites, promoting inflammation. The pro-inflammatory effects of Ang II are mediated by Ang II type I receptor (AT1), which stimulates aldosterone secretion from the adrenal medulla and antidiuretic hormone from the posterior pituitary. Aldosterone decreases membrane ACE2 expression. Endothelin-1 inhibits angiotensin 1-7 (Ang1-7) via extracellular signal-regulated kinase (ERK)1/ERK2 pathways. Ang II, under favorable conditions (dashed line), can be converted to Ang1-7 via ACE2, whose counter regulatory effects are mediated by the Mas receptor. Ang1-7 can also be formed via conversion of Ang I to an intermediate Ang1-9 or directly via zinc metallopeptidase neprilysin/prolyl endopeptidase (PEP). RAS = renin-angiotensin system."}

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