Evidence map›Paper›PMID 41515937›Full record

ArticleInternational journal of molecular sciences2025

Potential Cardioprotective Effect of a GRK5 Inhibitor Against NF-κB-Mediated Inflammation in an Animal Model of Isoproterenol-Induced Myocardial Infarction.

Asma S Alonazi, Anfal F Bin Dayel, Bashayer A Alkhathlan, Lulu M Alkaff, Ahad T Alrashed, Reema A Bin Klaib, Doaa M Elnagar, Maha A Alamin, Rehab A Ali, Alaa Alnoor Alameen and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Asma S AlonaziDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0003-3367-002X
Anfal F Bin DayelDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-7138-414X
Bashayer A AlkhathlanDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0009-0002-3981-1233
Lulu M AlkaffDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Ahad T AlrashedDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Reema A Bin KlaibDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Doaa M ElnagarZoology Department, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.
Maha A AlaminDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-4847-0840
Rehab A AliDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Alaa Alnoor AlameenDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-4073-2375
Nouf M AlrasheedDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0001-5283-1576

Funding

Ongoing Research Funding Program, King Saud University, Riyadh, Saudi Arabia. (ORF-2025-1218)
6 · The paper itself

Abstract

Myocardial infarction (MI) is a pathological condition associated with various cardiovascular diseases and leads to heart failure. Nuclear factor-kappa B (NF-κB) is upregulated in the infarcted heart. G protein-coupled receptor kinase 5 (GRK5) also plays a complex role in both tissue repair and maladaptive hypertrophy in cardiovascular diseases; however, its effect on NF-κB-mediated inflammation has not yet been elucidated. Thus, this study aims to investigate the effects of Amlexanox (AMX), a potential GRK5 inhibitor, in an animal model of MI by assessing its impact on GRK5-mediated NF-κB/inflammatory processes. Thirty-two male mice were randomly allocated into four groups: control, MI, (MI treated with vehicle (MI + V), and MI + AMX (AMX: 2.5 mg/100 g/day). MI was induced using ISO on days 21 and 22. The cardioprotective impacts of Amlexanox were verified by evaluating cardiac injury, inflammatory biomarker concentrations, and histopathological alterations in cardiomyocytes. MI induction was confirmed by increases in heart weight/body weight ratio (HW/BW) (

Indexed as

Cardiotonic AgentsG-Protein-Coupled Receptor Kinase 5InflammationMyocardial InfarctionNF-kappa BAminopyridinesAnimalsDisease Models, AnimalInterleukin-6IsoproterenolMaleMiceMyocytes, CardiacSignal TransductionAminopyridinesamlexanoxCardiotonic AgentsG-Protein-Coupled Receptor Kinase 5Grk5 protein, mouseInterleukin-6IsoproterenolNF-kappa BAmlexanoxGRK5inflammationmyocardial infarctionNF-κB

Identifiers

PMID41515937
PMCPMC12786180

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Registered trials

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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.