scholarly journals Activation of angiotensin‐converting enzyme 2/angiotensin (1–7)/mas receptor axis triggers autophagy and suppresses microglia proinflammatory polarization via forkhead box class O1 signaling

Aging Cell ◽  
2021 ◽  
Author(s):  
Ruili Dang ◽  
Mengqi Yang ◽  
Changmeng Cui ◽  
Changshui Wang ◽  
Wenyuan Zhang ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Mas Receptor ◽  
Forkhead Box

The angiotensin converting enzyme 2/angiotensin-(1-7)/Mas Receptor axis as a key player in alveolar bone remodeling

Bone ◽  
2019 ◽  
Vol 128 ◽  
pp. 115041 ◽  
Author(s):  
Celso Martins Queiroz-Junior ◽  
Anna Clara Paiva Menezes Santos ◽  
Izabela Galvão ◽  
Giovanna Ribeiro Souto ◽  
Ricardo Alves Mesquita ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Bone Remodeling ◽  
Alveolar Bone ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Mas Receptor ◽  
Alveolar Bone Remodeling

Targeting angiotensin-converting enzyme 2 as a new therapeutic target for cardiovascular diseases

2014 ◽  
Vol 92 (7) ◽  
pp. 558-565 ◽  
Author(s):  
Nirmal Parajuli ◽  
Tharmarajan Ramprasath ◽  
Vaibhav B. Patel ◽  
Wang Wang ◽  
Brendan Putko ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Angiotensin Converting Enzyme ◽  
Therapeutic Target ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Heart Failure Patients ◽  
Positive Effects ◽  
Mas Receptor

Angiotensin-converting enzyme 2 (ACE2) is a monocarboxypeptidase that metabolizes several vasoactive peptides, including angiotensin II (Ang-II; a vasoconstrictive/proliferative peptide), which it converts to Ang-(1–7). Ang-(1–7) acts through the Mas receptor to mediate vasodilatory/antiproliferative actions. The renin–angiotensin system involving the ACE–Ang-II–Ang-II type-1 receptor (AT1R) axis is antagonized by the ACE2–Ang-(1–7)–Mas receptor axis. Loss of ACE2 enhances adverse remodeling and susceptibility to pressure and volume overload. Human recombinant ACE2 may act to suppress myocardial hypertrophy, fibrosis, inflammation, and diastolic dysfunction in heart failure patients. The ACE2–Ang-(1–7)–Mas axis may present a new therapeutic target for the treatment of heart failure patients. This review is mainly focused on the analysis of ACE2, including its influence and potentially positive effects, as well as the potential use of human recombinant ACE2 as a novel therapy for the treatment cardiovascular diseases, such as hypertension and heart failure.

Angiotensin-(1-7), angiotensin-converting enzyme 2 and Mas receptor in rat polycystic ovaries

2020 ◽  
Vol 27 ◽  
Author(s):  
Virginia M. Pereira ◽  
Fernando M. Reis ◽  
Maíra Casalechi ◽  
Adelina M. Reis
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Polycystic Ovary ◽  
Renin Angiotensin System ◽  
Cyst Formation ◽  
Converting Enzyme ◽  
Polycystic Ovaries ◽  
Angiotensin Converting Enzyme 2 ◽  
Mas Receptor ◽  
Peptide System

Background: Hyperandrogenism is a pivotal mediator in the pathogenesis of the polycystic ovary syndrome (PCOS), but the mechanisms of androgen excess in this condition are not fully understood. Angiotensin (Ang)-(1-7) is an active peptide of the renin-angiotensin system (RAS) that stimulates ovarian follicular growth and testosterone release in vitro. Objective: To investigate whether Ang-(1-7), its receptor Mas and angiotensin-converting enzyme 2 (ACE2), the enzyme that converts Ang II into Ang-(1-7), are expressed in rat polycystic ovaries (PCO) and thus if this peptide system might be associated with excess androgen production in PCO. Methods: A rat model that shares some features of PCOS such as disruption of folliculogenesis and multiple ovarian cyst formation was used in the study. Results: We found reduced levels of Ang-(1-7) and Mas receptor in PCO compared to normal ovaries. Also, ACE2 mRNA expression was reduced in PCO compared to ovaries of control rats (p < 0.05). PCO had high levels of estrogen and testosterone and increased mRNA for upstream enzymes of the steroidogenic cascade, but not of P450 aromatase. Conclusion: These findings suggest that the ovarian ACE2-Ang-(1-7)-Mas receptor axis is inhibited and therefore may not be a co-factor of excess testosterone production in rat PCO.

Sign in / Sign up

Export Citation Format

Share Document