| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T626 |
0-144 |
Sentence |
denotes |
The renin-angiotensin aldosterone system (RAAS) is a key regulator of vascular function modulating natriuresis, blood volume and blood pressure. |
| T627 |
145-282 |
Sentence |
denotes |
Briefly, angiotensin I (Ang I) is metabolized by angiotensin-converting enzyme (ACE) to form the vasoconstrictor angiotensin II (Ang II). |
| T628 |
283-606 |
Sentence |
denotes |
Accumulation, prolonged and excessive binding of Ang II to the angiotensin 1 receptor in the heart and blood vessels mediates several effects which include vasoconstriction, hypertension, cardiac hypertrophy, increased ROS production and adverse fibrosis (Fyhrquist, Metsarinne, & Tikkanen, 1995; Perazella & Setaro, 2003). |
| T629 |
607-828 |
Sentence |
denotes |
Earlier literature demonstrated Ang II may act as a proinflammatory cytokine potentially having a significant role in cardiac remodeling (Gibbons, Pratt, & Dzau, 1992; Griendling, Minieri, Ollerenshaw, & Alexander, 1994). |
| T630 |
829-1194 |
Sentence |
denotes |
Conversely, the master regulator ACE2, a type 1 integral membrane glycoprotein expressed in most tissues including the lungs, kidneys, heart and vascular endothelium layers, can metabolize Ang II to produce the vasodilator angiotensin (Ang 1–7) which protects the cardiovascular system against the actions of Ang II (Das, 2018; Kumar & Das, 1997; Yan et al., 2020). |
| T631 |
1195-1564 |
Sentence |
denotes |
Beside its vasodilatory properties, Ang-(1–7) promotes resolution of inflammation by decreasing TNF-α, IL-6, vascular adhesion molecule, monocyte chemoattractant protein-1 and macrophage infiltration enhancing the survival of cardiomyocytes and endothelial cells during severe immune responses (Simoes e Silva, Silveira, Ferreira, & Teixeira, 2013; Zhang et al., 2015). |
| T632 |
1565-1783 |
Sentence |
denotes |
Accordingly, several clinical and experimental studies reported dysregulation of RAAS due to increased Ang II and decreased ACE2 can lead to detrimental inflammatory responses and worsening of cardiovascular disorders. |
| T633 |
1784-2096 |
Sentence |
denotes |
Therefore, maintaining the activity of ACE2 is essential in preserving the balance of the RAAS and effects on vasoconstriction, sodium retention and fibrosis and may elicit protective effects against hypertension, HF, MI and other CVDs (Crackower et al., 2002; Patel et al., 2016; Wang, Gheblawi, & Oudit, 2020). |
