LitCovid-sentences  

PMC:7161517 / 10011-11799 JSONTXT 11 Projects

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Id Subject Object Predicate Lexical cue
T70 55-194 Sentence denotes Normally, angiotensin I (Ang I) is converted to Ang II via angiotensin-converting enzyme (ACE), which could be inhibited by ACE inhibitors.
T71 195-276 Sentence denotes The pro-inflammatory effects of Ang II are mediated through AT1R in several ways:
T72 277-762 Sentence denotes 1) in the zona glomerulosa of the adrenal medulla, it stimulates aldosterone secretion and binding to mineralocorticoid receptors to promote water reabsorption and to increase salt retention; it is inhibited by mineralocorticoid receptor antagonists (MRAs); 2) in the posterior pituitary, Ang II stimulates antidiuretic hormone secretion to promote water retention; and 3) in other tissues, it stimulates pathways responsible for hypertrophy, fibrosis, oxidative stress, and apoptosis.
T73 763-868 Sentence denotes These effects are attenuated by angiotensin receptor blockers (ARBs), which block Ang II binding to AT1R.
T74 869-1008 Sentence denotes Ang II can also be converted to angiotensin 1-7 (Ang 1-7) via ACE2, which stimulates the Mas receptor promoting anti-inflammatory benefits.
T75 1009-1121 Sentence denotes The ACE2/Ang1-7/Mas axis acts as a counter regulatory pathway to the traditional renin-angiotensin system (RAS).
T76 1122-1148 Sentence denotes AT1R and ACE2 are coupled.
T77 1149-1227 Sentence denotes Ang II binding to AT1R allows dissociation of ACE2 and subsequent degradation.
T78 1228-1330 Sentence denotes ARB prevents dissociation of ACE2 and renders it availability for unused Ang II conversion to Ang 1-7.
T79 1331-1466 Sentence denotes ACE2 has been identified as the targeted receptor for both the severe acute respiratory syndrome coronavirus (SARS-CoV) 2 and SARS-CoV.
T80 1467-1597 Sentence denotes ACE2 mediates S protein binding that stimulates viral entry into the host cytosol that results in infection and viral replication.
T81 1598-1788 Sentence denotes Diversion of Ang II towards ACE2 could competitively inhibit viral binding and also counter regulate the adverse effects caused by AT1R and improve outcomes by Mas R−based favorable effects.