ReviewJournal of molecular medicine (Berlin, Germany)2003
A story of two ACEs.
Review in Journal of molecular medicine (Berlin, Germany), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- ACE2 gene polymorphism and essential hypertension: an updated meta-analysis involving 11,051 subjects.Molecular biology reports · 2012Pooled it
- ACE2, CALM3 and TNNI3K polymorphisms as potential disease modifiers in hypertrophic and dilated cardiomyopathies.Molecular and cellular biochemistry · 2018Trial
- Angiotensin‑converting enzyme 2 expression in human tumors: Implications for prognosis and therapy (Review).Oncology reports · 2025Review
- Progress of ADAM17 in Fibrosis-Related Diseases.Mediators of inflammation · 2025Review
- Rabbit and Human Angiotensin-Converting Enzyme-2: Structure and Electric Properties.International journal of molecular sciences · 2024Article
- Protective neutralizing epitopes in SARS-CoV-2.Immunological reviews · 2022Review
- An update on angiotensin-converting enzyme 2 structure/functions, polymorphism, and duplicitous nature in the pathophysiology of coronavirus disease 2019: Implications for vascular and coagulation disease associated with severe acute respiratory syndrome coronavirus infection.Frontiers in microbiology · 2022Review
- CD209L/L-SIGN and CD209/DC-SIGN Act as Receptors for SARS-CoV-2.ACS central science · 2021Article
- CD209L/L-SIGN and CD209/DC-SIGN act as receptors for SARS-CoV-2.bioRxiv : the preprint server for biology · 2021Article
- Dual role for angiotensin-converting enzyme 2 in Severe Acute Respiratory Syndrome Coronavirus 2 infection and cardiac fat.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2021Review
- Ozone therapy for the treatment of COVID-19 pneumonia: A scoping review.International immunopharmacology · 2021Article
- Article
- From ACE2 to COVID-19: A multiorgan endothelial disease.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2020Article
- The role of angiotensin-converting enzyme 2 in coronaviruses/influenza viruses and cardiovascular disease.Cardiovascular research · 2020Review
- COVID-19: Risk groups, mechanistic insights and challenges.International journal of clinical practice · 2020Article
- Angiotensin converting enzyme polymorphism and ischemic stroke.Neurosciences (Riyadh, Saudi Arabia) · 2020Article
- Review
- EZH2-mediated H3K27me3 inhibits ACE2 expression.Biochemical and biophysical research communications · 2020Article
- Angiotensin II mediates angiotensin converting enzyme type 2 internalization and degradation through an angiotensin II type I receptor-dependent mechanism.Hypertension (Dallas, Tex. : 1979) · 2014Article
- Angiotensin (1-7) contributes to nitric oxide tonic inhibition of vasopressin release during hemorrhagic shock in acute ethanol intoxicated rodents.Life sciences · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to the World Health Organization predictions cardiovascular diseases will be the leading cause of death by the year 2020. High blood pressure is a major risk factor for myocardial infarction, cerebrovascular disease, and stroke. Modulation of the renin-angiotensin system, particularly inhibition of the angiotensin-converting enzyme (ACE), has become a prime strategy in the treatment of hypertension and heart failure. Recently the gene of a new ACE, termed ACE2, has been characterized. The ACE2 gene maps to defined quantitative trait loci on the X chromosome in three different rat models of hypertension, suggesting ACE2 as a candidate gene for hypertension. In mice the targeted disruption of ACE2 resulted in increased systemic angiotensin II levels, impaired cardiac contractility, and upregulation of hypoxia-induced genes in the heart. Since mice deficient in both ACE2 and ACE show completely normal heart function, it appears that ACE and ACE2 negatively regulate each other. The mechanisms and physiological significance of the interplay between ACE and ACE2 are not yet elucidated, but it may involve several new peptides and peptide systems. In view of drug development the increasing complexity of the renin-angiotensin system offers both challenge and opportunity to develop new and refined treatment strategies against cardiovascular diseases.
Indexed as
Identifiers
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.