2020
DOI: 10.3389/fphys.2020.01067
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Role of Renin-Angiotensin System Components in Atherosclerosis: Focus on Ang-II, ACE2, and Ang-1–7

Abstract: Atherosclerosis is the leading cause of vascular disease worldwide and contributes significantly to deaths from cardiovascular complications. There is a remarkably close relationship between atherosclerotic plaque formation and the activation of renin-angiotensin system (RAS). However, depending on which RAS pathway is activated, pro-or anti-atherogenic outcomes may be observed. This brief review focuses on the role of three of the most important pieces of RAS axis, angiotensin II (Ang-II), angiotensin convert… Show more

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Cited by 44 publications
(46 citation statements)
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References 85 publications
(115 reference statements)
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“…It also plays a role in the adhesion of mononuclear cells to the arterial endothelium and recruitment of mononuclear cells by stimulating the increase in CAM expression of TNF-α, which is released as a result of stimulation of AT1R with AngII, in combination with IL-6 [35]. One study reported that AngII induced monocyte chemotactic protein-derived protein expression (MCPIP1) via an AMPK/p38 MAPK-dependent pathway [36]. Increased MCPIP1 expression contributes to atherosclerotic plaque formation by triggering apoptosis in macrophages [37].…”
Section: Atherosclerosismentioning
confidence: 99%
“…It also plays a role in the adhesion of mononuclear cells to the arterial endothelium and recruitment of mononuclear cells by stimulating the increase in CAM expression of TNF-α, which is released as a result of stimulation of AT1R with AngII, in combination with IL-6 [35]. One study reported that AngII induced monocyte chemotactic protein-derived protein expression (MCPIP1) via an AMPK/p38 MAPK-dependent pathway [36]. Increased MCPIP1 expression contributes to atherosclerotic plaque formation by triggering apoptosis in macrophages [37].…”
Section: Atherosclerosismentioning
confidence: 99%
“…Endothelial damage and inflammation allow for the migration of monocytes and macrophages to the site of injury and the formation of foam cells. [13][14][15]. Additionally, stimulation of inflammatory mediators also promotes smooth muscle cell (SMC) thickening, stiffness of vessels and forms a fibrous cap on the atherosclerotic plaque (Figure 2) [16].…”
Section: Atherosclerosis and Endothelial Dysfunctionmentioning
confidence: 99%
“…It occurs due to the gradual buildup of atherosclerotic plaque within the wall of arteries leading to reduced oxygen delivery to cardiac myocytes. It comprises a clinical spectrum based on the degree of luminal narrowing and the activation of the atherosclerotic plaque [13,14]. The RAAS plays a vital role in the pathogenesis of CAD.…”
Section: Ischemic Heart Diseasementioning
confidence: 99%
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“…Two G protein-coupled receptors mediate the effects of Ang- [1][2][3][4][5][6][7][8]. Excessive Ang- [1][2][3][4][5][6][7][8] activity at the angiotensin type 1 receptor (AT 1 R) leads to hypertension, inflammation, atherogenesis and tissue fibrosis (72,95). The angiotensin type 2 receptor (AT 2 R) plays a counter-regulatory role in AT 1 R actions, especially in the female (90,91).…”
Section: Introductionmentioning
confidence: 99%