ReviewFrontiers in endocrinology2014
Update on the Angiotensin converting enzyme 2-Angiotensin (1-7)-MAS receptor axis: fetal programing, sex differences, and intracellular pathways.
Review in Frontiers in endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04752293 (Pediatric Hypertension and the Renin-Angiotensin SystEm), which is not on this map. Cited by 129 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Pediatric Hypertension and the Renin-Angiotensin SystEm (PHRASE): The Role of Angiotensin-(1-7) in Hypertension and Hypertension-Induced Heart and Kidney Damage
Who cites it
129 citing papers in PubMed, 194 citations in OpenAlex.
- Severe Acute Hypertension Causes Hemolysis With Release of PEP and ACE Inhibitor.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Article
- Therapeutic Opportunities Targeting the ACE2/Ang-(1-7)/MasR Pathway in Cardiometabolic Disease.Current hypertension reports · 2026Review
- Novel aspects of the renin-angiotensin-aldosterone system in septic shock.Current opinion in physiology · 2026Article
- Analysis of modifying factors for ACE2 to work effectively.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- The circulating renin-angiotensin system and mortality among patients hospitalized for COVID-19: a mechanistic substudy of the ACTIV-4 Host Tissue trials.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- ACE2, From the Kidney to SARS-CoV-2: Donald Seldin Award Lecture 2023.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Kidney Programming and Hypertension: Linking Prenatal Development to Adulthood.International journal of molecular sciences · 2024Review
- Altered kidney distribution and loss of ACE2 into the urine in acute kidney injury.American journal of physiology. Renal physiology · 2024Article
- Lactoferrin Supplementation during Pregnancy and Lactation Protects Adult Male Rat Offspring from Hypertension Induced by Maternal Adenine Diet.Nutrients · 2024Article
- Review
- Renin in critically ill patients.Annals of intensive care · 2024Review
- The Renin-Angiotensin System and Cardiovascular-Kidney-Metabolic Syndrome: Focus on Early-Life Programming.International journal of molecular sciences · 2024Review
- Changes in nonfunctional adrenal incidentaloma after COVID-19 infection and a model for predicting benign and malignant adrenal incidentaloma.Frontiers in endocrinology · 2024Article
- Article
- Genotype variation of ACE and ACE2 genes affects the severity of COVID-19 patients.BMC research notes · 2023Article
- The Relationship between Renin-Angiotensin-Aldosterone System (RAAS) Activity, Osteoporosis and Estrogen Deficiency in Type 2 Diabetes.International journal of molecular sciences · 2023Review
- Renin-Angiotensin System and Sex Differences in COVID-19: A Critical Assessment.Circulation research · 2023Review
- Sex hormones in SARS-CoV-2 susceptibility: key players or confounders?Nature reviews. Endocrinology · 2023Review
- Controls of Central and Peripheral Blood Pressure and Hemorrhagic/Hypovolemic Shock.Journal of clinical medicine · 2023Review
69 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The renin-angiotensin-system (RAS) constitutes an important hormonal system in the physiological regulation of blood pressure. Indeed, dysregulation of the RAS may lead to the development of cardiovascular pathologies including kidney injury. Moreover, the blockade of this system by the inhibition of angiotensin converting enzyme (ACE) or antagonism of the angiotensin type 1 receptor (AT1R) constitutes an effective therapeutic regimen. It is now apparent with the identification of multiple components of the RAS that the system is comprised of different angiotensin peptides with diverse biological actions mediated by distinct receptor subtypes. The classic RAS can be defined as the ACE-Ang II-AT1R axis that promotes vasoconstriction, sodium retention, and other mechanisms to maintain blood pressure, as well as increased oxidative stress, fibrosis, cellular growth, and inflammation in pathological conditions. In contrast, the non-classical RAS composed of the ACE2-Ang-(1-7)-Mas receptor axis generally opposes the actions of a stimulated Ang II-AT1R axis through an increase in nitric oxide and prostaglandins and mediates vasodilation, natriuresis, diuresis, and oxidative stress. Thus, a reduced tone of the Ang-(1-7) system may contribute to these pathologies as well. Moreover, the non-classical RAS components may contribute to the effects of therapeutic blockade of the classical system to reduce blood pressure and attenuate various indices of renal injury. The review considers recent studies on the ACE2-Ang-(1-7)-Mas receptor axis regarding the precursor for Ang-(1-7), the intracellular expression and sex differences of this system, as well as an emerging role of the Ang1-(1-7) pathway in fetal programing events and cardiovascular dysfunction.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.