Angiotensin converting enzyme 2 and atherosclerosis

Wang, Yutang; Tikellis, Chris; Thomas, Merlin C.; Golledge, Jonathan

doi:10.1016/j.atherosclerosis.2012.08.018

Cited by 57 publications

(48 citation statements)

References 55 publications

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“…Indeed, previous studies have identified ACE2 as a negative regulator of the RAS by converting Ang II into Ang-(1-7), which, by acting via its own receptor Mas, can inhibit platelet adhesion and thrombosis formation, suppress inflammation, stabilize atherosclerotic plaques, promote myocardial remodeling and lower blood pressure. 8,[14][15][16] More recently, Ohshima et al found that elevated Ang-(1-7) expression could in turn upregulate the mRNA levels of ACE2 and ATR2 in the injured artery. 17 Their results suggested novel interactions between ACE2-Ang-(1-7)-Mas axis and ACE-Ang II-ATR2 axis in vascular remodeling and further revealed the multiple functions of ACE2 in protecting against the development and progression of vascular diseases.…”

Section: Discussionmentioning

confidence: 99%

Novel findings: Expression of angiotensin-converting enzyme and angiotensin-converting enzyme 2 in thoracic aortic dissection and aneurysm

Qian

et al. 2014

J Renin Angiotensin Aldosterone Syst

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Introduction: Angiotensin-converting enzyme (ACE) and ACE2 are key regulators of the renin–angiotensin system, which has been shown to participate in a series of cardiovascular diseases. We hypothesized that dysregulated gene expression of ACE and ACE2 contribute to the formation of thoracic aortic dissection and aneurysm. Materials and methods: We assessed ACE plasma concentration in 73 patients with acute thoracic aortic dissection (n=34), aneurysm (n=18), coronary heart disease (n=21) and 13 healthy volunteers. ACE and ACE2 gene expression in available aortic tissues was also examined by using quantitative real-time polymerase chain reaction. Results: In patients with acute aortic dissection, ACE plasma concentration and its mRNA level in aortic tissue were markedly reduced compared with those in patients with aneurysm, coronary heart disease and healthy controls. The level of ACE2 gene expression in dissection samples was also significantly lower than that in aneurysm (8.01±7.44, p<0.01) and coronary heart disease groups (9.61±11.54, p<0.01). A strong correlation was observed between the gene expressions of ACE and those of ACE2, and ACE to ACE2 ratio was significantly elevated in dissection tissues. Conclusions: Imbalanced down-regulation of ACE and ACE2 mRNA expression levels may play an important role in the development and progression of thoracic aortic aneurysmal dilatation and subsequently dissection.

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Section: Discussionmentioning

confidence: 99%

Novel findings: Expression of angiotensin-converting enzyme and angiotensin-converting enzyme 2 in thoracic aortic dissection and aneurysm

Qian

et al. 2014

J Renin Angiotensin Aldosterone Syst

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“…ACE2 and its product Ang-(1-7) have been reported to exert antiatherosclerotic properties, including decrease in inflammation and cell proliferation. 17 For instance, chronic Ang-(1-7) infusion induced improvement of endothelial cell function and inhibited atherosclerotic lesion formation in apolipoprotein E-deficient mice. 18 Furthermore, a recent study demonstrated that long-term Ang-(1-7) treatment dose dependently inhibited early atherosclerotic lesion formation through vascular smooth muscle cell proliferation and migration in apolipoprotein E-deficient mice.…”

Section: Discussionmentioning

confidence: 99%

Possible Role of Angiotensin-Converting Enzyme 2 and Activation of Angiotensin II Type 2 Receptor by Angiotensin-(1–7) in Improvement of Vascular Remodeling by Angiotensin II Type 1 Receptor Blockade

et al. 2014

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Cross talk between the angiotensin-converting enzyme (ACE)/angiotensin II (Ang II)/Ang II type 1 (AT 1 ) receptor axis and the ACE2/Ang-(1–7)/Mas axis plays a role in the pathogenesis of cardiovascular remodeling. Furthermore, possible stimulation of the Ang II type 2 (AT 2 ) receptor by Ang-(1–7) has been highlighted as a new pathway. Therefore, we examined the possibility of whether the ACE2/Ang-(1–7)/Mas axis and Ang-(1–7)/AT 2 receptor axis are involved in the inhibitory effects of AT 1 receptor blockers on vascular remodeling. Wild-type, Mas-knockout, and AT 2 receptor knockout mice were used in this study. Vascular injury was induced by polyethylene-cuff placement around the mouse femoral artery. Some mice were treated with azilsartan, an AT 1 receptor blocker, or Ang-(1–7). Neointimal formation 2 weeks after cuff placement was more marked in Mas-knockout mice compared with wild-type mice. Treatment with azilsartan or Ang-(1–7) attenuated neointimal area, vascular smooth muscle cell proliferation, increases in the mRNA levels of monocyte chemoattractant protein-1, tumor necrosis factor-α, and interleukin-1β, and superoxide anion production in the injured artery; however, these inhibitory effects of azilsartan and Ang-(1–7) were less marked in Mas-knockout mice. Administration of azilsartan or Ang-(1–7) attenuated the decrease in ACE2 mRNA and increased AT 2 receptor mRNA but did not affect AT 1 receptor mRNA or the decrease in Mas mRNA. The inhibitory effect of Ang-(1–7) on neointimal formation was less marked in AT 2 receptor knockout mice compared with wild-type mice. These results suggest that blockade of the AT 1 receptor by azilsartan could enhance the activities of the ACE2/Ang-(1–7)/Mas axis and ACE2/Ang-(1–7)/AT 2 receptor axis, thereby inhibiting neointimal formation.

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“…A wealth of evidence indicates that the renin-angiotensin system (RAS) is a crucial regulator of cardiovascular homeostasis and has an important role in the pathogenesis of endothelial dysfunction and atherosclerosis [1,2]. Previous studies have shown that adhesion molecular and inflammatory cytokines, for example, MCP-1, VCAM-1 and interleukin 6, are important molecules in the generation of endothelial dysfunction and induction of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

ACE2 and Ang-(1–7) protect endothelial cell function and prevent early atherosclerosis by inhibiting inflammatory response

et al. 2015

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Angiotensin converting enzyme 2 and atherosclerosis

Cited by 57 publications

References 55 publications

Novel findings: Expression of angiotensin-converting enzyme and angiotensin-converting enzyme 2 in thoracic aortic dissection and aneurysm

Novel findings: Expression of angiotensin-converting enzyme and angiotensin-converting enzyme 2 in thoracic aortic dissection and aneurysm

Possible Role of Angiotensin-Converting Enzyme 2 and Activation of Angiotensin II Type 2 Receptor by Angiotensin-(1–7) in Improvement of Vascular Remodeling by Angiotensin II Type 1 Receptor Blockade

ACE2 and Ang-(1–7) protect endothelial cell function and prevent early atherosclerosis by inhibiting inflammatory response

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