Evidence map›Paper›PMID 37365840›Full record

ReviewCell cycle (Georgetown, Tex.)2023

Mas receptor: a potential strategy in the management of ischemic cardiovascular diseases.

Ali Molaei, Emad Molaei, A Wallace Hayes, Gholamreza Karimi

Open access · greenAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  6. Gestational arsenite exposure alters maternal postpartum heart size and induces CaAmerican journal of physiology. Heart and circulatory physiology · 2025
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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

4 authors at 3 institutions in 2 countries.

Ali MolaeiFaculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Emad MolaeiPharmD, Assistant of Clinical Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
A Wallace HayesUniversity of South Florida College of Public Health, Tampa, Florida, USA.
Gholamreza KarimiPharmaceutical Research Center, Institute of Pharmaceutical Technology, Mashhad University of Medical Sciences, Mashhad, Iran.
Mashhad University of Medical Sciences · IRTehran University of Medical Sciences · IRUniversity of South Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MasR is a critical element in the RAS accessory pathway that protects the heart against myocardial infarction, ischemia-reperfusion injury, and pathological remodeling by counteracting the effects of AT1R. This receptor is mainly stimulated by Ang 1-7, which is a bioactive metabolite of the angiotensin produced by ACE2. MasR activation attenuates ischemia-related myocardial damage by facilitating vasorelaxation, improving cell metabolism, reducing inflammation and oxidative stress, inhibiting thrombosis, and stabilizing atherosclerotic plaque. It also prevents pathological cardiac remodeling by suppressing hypertrophy- and fibrosis-inducing signals. In addition, the potential of MasR in lowering blood pressure, improving blood glucose and lipid profiles, and weight loss has made it effective in modulating risk factors for coronary artery disease including hypertension, diabetes, dyslipidemia, and obesity. Considering these properties, the administration of MasR agonists offers a promising approach to the prevention and treatment of ischemic heart disease.

Indexed as

Cardiovascular DiseasesCoronary Artery DiseaseAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsAngiotensinsChemokinesHumansIschemiaLigandsAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsAngiotensinsChemokinesLigandsAng 1-7AtherosclerosisDiabetesIschemic heart diseaseMasRObesity

Identifiers

PMID37365840
PMCPMC10361149
OpenAlexW4382181916

What OpenQuestion holds

Textmetadata
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.