Evidence map›Paper›PMID 26631237›Full record

ReviewDrugs2016

Combined Angiotensin Receptor Modulation in the Management of Cardio-Metabolic Disorders.

Ludovit Paulis, Sébastien Foulquier, Pawel Namsolleck, Chiara Recarti, Ulrike Muscha Steckelings, Thomas Unger

Open access · hybridAbstract readReview
In one paragraph

Review in Drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Lipotoxicity-Related Hematological Disorders in Obesity.Advances in experimental medicine and biology · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Activation of ATBritish journal of pharmacology · 2020
    Article
  8. Article
  9. Article
  10. Angiotensin Type 2 Receptors: Painful, or Not?Frontiers in pharmacology · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Ludovit PaulisFaculty of Medicine, Institute of Pathological Physiology, Comenius University in Bratislava, Sasinkova 4, 81108, Bratislava, Slovak Republic.
Sébastien FoulquierCARIM-School for Cardiovascular Diseases, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands.
Pawel NamsolleckCARIM-School for Cardiovascular Diseases, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands.
Chiara RecartiCARIM-School for Cardiovascular Diseases, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands.
Ulrike Muscha SteckelingsInstitute of Molecular Medicine-Department of Cardiovascular and Renal Research, University of Southern Denmark, 5000, Odense, Denmark.
Thomas UngerCARIM-School for Cardiovascular Diseases, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands. t.unger@maastrichtuniversity.nl.
Maastricht University · NLComenius University Bratislava · SKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular and metabolic disorders, such as hypertension, insulin resistance, dyslipidemia or obesity are linked with chronic low-grade inflammation and dysregulation of the renin-angiotensin system (RAS). Consequently, RAS inhibition by ACE inhibitors or angiotensin AT1 receptor (AT1R) blockers is the evidence-based standard for cardiovascular risk reduction in high-risk patients, including diabetics with albuminuria. In addition, RAS inhibition reduces the new onset of diabetes mellitus. Yet, the high and increasing prevalence of metabolic disorders, and the high residual risk even in properly treated patients, calls for additional means of pharmacological intervention. In the past decade, the stimulation of the angiotensin AT2 receptor (AT2R) has been shown to reduce inflammation, improve cardiac and vascular remodeling, enhance insulin sensitivity and increase adiponectin production. Therefore, a concept of dual AT1R/AT2R modulation emerges as a putative means for risk reduction in cardio-metabolic diseases. The approach employing simultaneous RAS blockade (AT1R) and RAS stimulation (AT2R) is distinct from previous attempts of double intervention in the RAS by dual blockade. Dual blockade abolishes the AT1R-linked RAS almost completely with subsequent risk of hypotension and hypotension-related events, i.e. syncope or renal dysfunction. Such complications might be especially prominent in patients with renal impairment or patients with isolated systolic hypertension and normal-to-low diastolic blood pressure values. In contrast to dual RAS blockade, the add-on of AT2R stimulation does not exert significant blood pressure effects, but it may complement and enhance the anti-inflammatory and antifibrotic/de-stiffening effects of the AT1R blockade and improve the metabolic profile. Further studies will have to investigate these putative effects in particular for settings in which blood pressure reduction is not primarily desired.

Indexed as

Angiotensin II Type 1 Receptor BlockersCardiovascular DiseasesDrug Therapy, CombinationHumansInflammationMetabolic DiseasesReceptor, Angiotensin, Type 2Renin-Angiotensin SystemAngiotensin II Type 1 Receptor BlockersReceptor, Angiotensin, Type 2

Identifiers

PMID26631237
PMCPMC4700059
OpenAlexW2185635160

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.