Decreased levels of serum Angiotensin-(1–7) in patients with pulmonary arterial hypertension due to congenital heart disease

Dai, Hai-Long; Gong, Yongfei; Xiao, Zhicheng; Xue-feng, Guang; Yin, Xianzhen

doi:10.1016/j.ijcard.2014.08.021

Cited by 21 publications

(16 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Decreased lung ACE2 expression 79,80 and enzymatic activity 81 , along with increased circulating Ang II levels 82 , have been observed in PAH. Additionally, reduction in circulating ACE2 and Ang-(1-7) levels has been observed in patients with PAH from congenital HD 83,84 . Moreover, auto-antibodies to ACE2 predisposed patients with connective tissue diseases to development of PAH 85 .…”

Section: Ace2 In Pulmonary Arterial Hypertensionmentioning

confidence: 98%

ACE2 and Microbiota

Cole‐Jeffrey

Katovich

et al. 2015

Journal of Cardiovascular Pharmacology

102

View full text Add to dashboard Cite

The health of the cardiovascular and pulmonary systems is inextricably linked to the renin-angiotensin system (RAS). Physiologically speaking, a balance between the vasodeleterious (ACE/Ang II/AT1R) and vasoprotective (ACE2/Ang-(1–7)/MasR) components of the RAS is critical for cardiopulmonary homeostasis. Upregulation of the ACE/Ang II/AT1R axis shifts the system toward vasoconstriction, proliferation, hypertrophy, inflammation, and fibrosis, all factors that contribute to the development and progression of cardiopulmonary diseases. Conversely, stimulation of the vasoprotective ACE2/Ang-(1–7)/MasR axis produces a counter-regulatory response that promotes cardiovascular health. Current research is investigating novel strategies to augment actions of the vasoprotective RAS components, particularly ACE2, in order to treat various pathologies. While multiple approaches to increase the activity of ACE2 have displayed beneficial effects against experimental disease models, the mechanisms behind its protective actions remain incompletely understood. Recent work demonstrating a non-catalytic role for ACE2 in amino acid transport in the gut has led us to speculate that the therapeutic effects of ACE2 can be mediated, in part, by its actions on the gastrointestinal tract and/or gut microbiome. This is consistent with emerging data which suggests that dysbiosis of the gut and lung microbiomes is associated with cardiopulmonary disease. This review highlights new developments in the protective actions of ACE2 against cardiopulmonary disorders, discusses innovative approaches to targeting ACE2 for therapy, and explores an evolving role for gut and lung microbiota in cardiopulmonary health.

show abstract

Section: Ace2 In Pulmonary Arterial Hypertensionmentioning

confidence: 98%

ACE2 and Microbiota

Cole‐Jeffrey

Katovich

et al. 2015

Journal of Cardiovascular Pharmacology

102

View full text Add to dashboard Cite

show abstract

“…Since the demonstration of the beneficial effects of the ACE2/ANG-(1-7)/MAS axis in pulmonary arterial hyper-tension (PAH) by Shenoy et al (497), emerging evidence has suggested that ANG-(1-7) has a protective role in this condition (498). Its importance in PAH comes from the observation that in patients with PAH from congenital heart disease, the peptide is reduced in plasma (110). The significant smaller response shown by TGR(mREN2)27 rats than SD to chronic hypoxia was related to the increased expression of ACE2 in the lung, leading to ACE2 activity and especially to markedly increased lung ANG-(1-7) concentrations and MAS expression in this strain (236).…”

Section: E Lungmentioning

confidence: 99%

The ACE2/Angiotensin-(1–7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1–7)

Santos

Sampaio

Alzamora

et al. 2018

Physiological Reviews

887

906

View full text Add to dashboard Cite

The renin-angiotensin system (RAS) is a key player in the control of the cardiovascular system and hydroelectrolyte balance, with an influence on organs and functions throughout the body. The classical view of this system saw it as a sequence of many enzymatic steps that culminate in the production of a single biologically active metabolite, the octapeptide angiotensin (ANG) II, by the angiotensin converting enzyme (ACE). The past two decades have revealed new functions for some of the intermediate products, beyond their roles as substrates along the classical route. They may be processed in alternative ways by enzymes such as the ACE homolog ACE2. One effect is to establish a second axis through ACE2/ANG-(1-7)/MAS, whose end point is the metabolite ANG-(1-7). ACE2 and other enzymes can form ANG-(1-7) directly or indirectly from either the decapeptide ANG I or from ANG II. In many cases, this second axis appears to counteract or modulate the effects of the classical axis. ANG-(1-7) itself acts on the receptor MAS to influence a range of mechanisms in the heart, kidney, brain, and other tissues. This review highlights the current knowledge about the roles of ANG-(1-7) in physiology and disease, with particular emphasis on the brain.

show abstract

“…Increased AngII levels without changes in Ang-(1-7) levels were found in the serum of 11 idiopathic or heritable PAH patients [7]. Decreased levels of serum ACE2 and Ang-(1-7) in patients with PAH due to congenital heart disease were also reported [20,21]. Consistent with this notion of an imbalanced ACE/ACE2 ratio in PAH patients, ZHANG et al [3] have recently reported that the expression and phosphorylation status (Ser-680) of ACE2 were markedly decreased in remodelled pulmonary arteries in explanted lung sections from patients with iPAH.…”

Section: Dysregulation Of Circulating and Local Ras And Potential Thementioning

confidence: 85%