Evidence mapPaperPMID 41970431Full record

ReviewHealth science reports2026

Potential Effects of Aspirin on Transcription Factors Related to the Inflammation in Atherosclerosis: A Systematic Review.

Mojtaba Aghaei, Reyhane Khademi, Seyed Sobhan Bahreiny, Habib Haybar, Ekhlas Torfi, Shirin Azizidoost, Najmaldin Saki

Abstract readReview
In one paragraph

Review in Health science reports, 2026. 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

7 authors.

Mojtaba AghaeiThalassemia & Hemoglobinopathy Research Center, Health Research Institute Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.ORCID https://orcid.org/0000-0002-6382-6657
Reyhane KhademiThalassemia & Hemoglobinopathy Research Center, Health Research Institute Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.ORCID https://orcid.org/0000-0003-3121-9307
Seyed Sobhan BahreinyStudent Research Committee Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.ORCID https://orcid.org/0000-0003-2148-1205
Habib HaybarAtherosclerosis Research Center Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.ORCID https://orcid.org/0000-0003-2202-6538
Ekhlas TorfiDepartment of Cardiovascular Disease, School of Medicine Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.ORCID https://orcid.org/0000-0003-0351-3541
Shirin AzizidoostAtherosclerosis Research Center Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.ORCID https://orcid.org/0000-0001-6102-3263
Najmaldin SakiThalassemia & Hemoglobinopathy Research Center, Health Research Institute Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.ORCID https://orcid.org/0000-0001-8494-5594

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Atherosclerosis (AS), a major cause of cardiovascular mortality, involves chronic inflammation mediated by transcription factors such as NF-κB, PPARs, and AP-2α. Beyond its antiplatelet role, aspirin exerts anti-inflammatory effects that may influence these molecular pathways. This review systematically evaluates aspirin's modulatory effects on these transcription factors in AS. Methods: Relevant English-language studies (1980-2025) were retrieved from PubMed, ScienceDirect, and Google Scholar using keywords related to aspirin, atherosclerosis, and inflammation-related transcription factors. Results: Aspirin inhibits NF-κB activation, reduces proinflammatory cytokine production, and enhances PPAR and AP-2α signaling, contributing to anti-inflammatory and plaque-stabilizing effects. Clinical findings (e.g., ARRIVE, ASPREE) show variable cardiovascular outcomes, likely reflecting dose- and population-dependent responses. Conclusion: Aspirin modulates key inflammatory transcription factors in AS, offering potential benefits beyond platelet inhibition. Further studies should clarify AP-2α's mechanistic role and explore aspirin-based combination strategies tailored to patient-specific inflammatory profiles.

Indexed as

AP‐2αaspirinatherosclerosisNF‐κBPPAR

Identifiers

PMID41970431
PMCPMC13062501

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.