Does ACE2 contribute to the development of hypertension?

Chappell, Mark C.

doi:10.1038/hr.2009.207

Cited by 10 publications

(8 citation statements)

References 22 publications

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“…53), Ang-(1-9), which enhances bradykinin actions, NO production and platelet regulation (Ref. 54), and Ang-(1-12), implicated in cardiac function (Ref. 55).…”

Section: The Ras – An Updatementioning

confidence: 99%

Angiotensin II and the vascular phenotype in hypertension

Savoia

Burger

Nishigaki

et al. 2011

Expert Rev. Mol. Med.

169

102

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Hypertension is associated with vascular changes characterised by remodelling, endothelial dysfunction and hyperreactivity. Cellular processes underlying these perturbations include altered vascular smooth muscle cell growth and apoptosis, fibrosis, hypercontractility and calcification. Inflammation, associated with macrophage infiltration and increased expression of redox-sensitive pro-inflammatory genes, also contributes to vascular remodelling. Many of these features occur with ageing, and the vascular phenotype in hypertension is considered a phenomenon of 'premature vascular ageing'. Among the many factors involved in the hypertensive vascular phenotype, angiotensin II (Ang II) is especially important. Ang II, previously thought to be the sole effector of the renin-angiotensin system (RAS), is converted to smaller peptides [Ang III, Ang IV, Ang-(1-7)] that are biologically active in the vascular system. Another new component of the RAS is the (pro)renin receptor, which signals through Ang-II-independent mechanisms and might influence vascular function. Ang II mediates effects through complex signalling pathways on binding to its G-protein-coupled receptors (GPCRs) AT1R and AT2R. These receptors are regulated by the GPCR-interacting proteins ATRAP, ARAP1 and ATIP. AT1R activation induces effects through the phospholipase C pathway, mitogen-activated protein kinases, tyrosine kinases/phosphatases, RhoA/Rhokinase and NAD(P)H-oxidase-derived reactive oxygen species. Here we focus on recent developments and new research trends related to Ang II and the RAS and involvement in the hypertensive vascular phenotype.

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“…53), Ang-(1-9), which enhances bradykinin actions, NO production and platelet regulation (Ref. 54), and Ang-(1-12), implicated in cardiac function (Ref. 55).…”

Section: The Ras – An Updatementioning

confidence: 99%

Angiotensin II and the vascular phenotype in hypertension

Savoia

Burger

Nishigaki

et al. 2011

Expert Rev. Mol. Med.

169

102

View full text Add to dashboard Cite

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“…The alternative pathway of Ang-(1–7) generation in the kidney includes degradation of Ang II by ACE2 which is highly expressed in the kidney (Chappell, 2010; Shaltout et al, 2009). Several reports showed that ACE and ACE2 colocalize on the apical surface of the proximal tubules while ACE2 is expressed in podocytes and parietal epithelial cells of the Bowman’s capsule within the glomerulus (Li et al, 2005; Wysocki et al, 2006; Ye et al, 2006).…”

Section: The Ace2/ang-(1–7)/mas Axismentioning

confidence: 99%

Advances in the Renin Angiotensin System

Ferrario

Ahmad²,

Joyner³

et al. 2010

Advances in Pharmacology

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The contribution of the renin angiotensin system to physiology and pathology is undergoing a rapid reconsideration of its mechanisms from emerging new concepts implicating angiotensin-converting enzyme 2 and angiotensin-(1–7) as new elements negatively influencing the vasoconstrictor, trophic, and pro-inflammatory actions of angiotensin II. This component of the system acts to oppose the vasoconstrictor and proliferative effects on angiotensin II through signaling mechanisms mediated by the mas receptor. In addition, a reduced expression of the vasodepressor axis composed by angiotensin-converting enzyme 2 and angiotensin-(1–7) may contribute to the expression of essential hypertension, the remodeling of heart and renal function associated with this disease, and even the physiology of pregnancy and the development of eclampsia.

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“…that could indirectly result in hypertension (42,45,46). These support the contrasting effects of ACE2/Ang (1-7) and ACE/Ang II axes (42,45,46).…”

Section: Ace2 Cleavage and The Enzymes Involvedmentioning

confidence: 54%

“…However, deletion of Ace2 expression in mouse model did not directly cause hypertension but caused enhanced susceptibility to Ang II-induced hypertension ( 44 ). Moreover, reduced ACE2 expression is associated with cardiac dysfunction and heart failure that could indirectly result in hypertension ( 42 , 45 , 46 ). These support the contrasting effects of ACE2/Ang (1-7) and ACE/Ang II axes ( 42 , 45 , 46 ).…”

Section: Ace2 Cleavage and The Enzymes Involvedmentioning

confidence: 99%

Regulated Intramembrane Proteolysis of ACE2: A Potential Mechanism Contributing to COVID-19 Pathogenesis?

González

Siddik

2021

Front. Immunol.

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Since being identified as a key receptor for SARS-CoV-2, Angiotensin converting enzyme 2 (ACE2) has been studied as one of the potential targets for the development of preventative and/or treatment options. Tissue expression of ACE2 and the amino acids interacting with the spike protein of SARS-CoV-2 have been mapped. Furthermore, the recombinant soluble extracellular domain of ACE2 is already in phase 2 trials as a treatment for SARS-CoV-2 infection. Most studies have continued to focus on the ACE2 extracellular domain, which is known to play key roles in the renin angiotensin system and in amino acid uptake. However, few also found ACE2 to have an immune-modulatory function and its intracellular tail may be one of the signaling molecules in regulating cellular activation. The implication of its immune-modulatory role in preventing the cytokine-storm, observed in severe COVID-19 disease outcomes requires further investigation. This review focuses on the regulated proteolytic cleavage of ACE2 upon binding to inducer(s), such as the spike protein of SARS-CoV, the potential of cleaved ACE2 intracellular subdomain in regulating cellular function, and the ACE2’s immune-modulatory function. This knowledge is critical for targeting ACE2 levels for developing prophylactic treatment or preventative measures in SARS-CoV infections.

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Does ACE2 contribute to the development of hypertension?

Cited by 10 publications

References 22 publications

Angiotensin II and the vascular phenotype in hypertension

Angiotensin II and the vascular phenotype in hypertension

Advances in the Renin Angiotensin System

Regulated Intramembrane Proteolysis of ACE2: A Potential Mechanism Contributing to COVID-19 Pathogenesis?

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