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

Mojtaba Aghaei1,2,3, Reyhane Khademi1,3, Seyed Sobhan Bahreiny2

  • 1Thalassemia & Hemoglobinopathy Research Center, Health Research Institute Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran.

Health Science Reports
|April 13, 2026
PubMed

Insights

Aspirin reduces inflammation in atherosclerosis by modulating key transcription factors like NF-κB and PPARs. This review highlights aspirin's anti-inflammatory actions beyond its antiplatelet effects for cardiovascular health.

Area of Science:

  • Cardiovascular Research
  • Inflammation Biology
  • Pharmacology

Background:

  • Atherosclerosis (AS) is a leading cause of cardiovascular death, driven by chronic inflammation.
  • Transcription factors, including NF-κB, PPARs, and AP-2α, are central to AS inflammatory pathways.
  • Aspirin, known for antiplatelet effects, also possesses anti-inflammatory properties relevant to AS.

Purpose of the Study:

  • To systematically review aspirin's effects on key inflammation-related transcription factors in atherosclerosis.
  • To evaluate how aspirin modulates NF-κB, PPARs, and AP-2α signaling in the context of AS.
  • To explore aspirin's potential anti-inflammatory mechanisms in AS beyond its antiplatelet function.

Main Methods:

  • Comprehensive literature search of PubMed, ScienceDirect, and Google Scholar (1980-2025).
  • Inclusion of English-language studies using keywords: aspirin, atherosclerosis, inflammation, NF-κB, PPARs, AP-2α.
  • Systematic evaluation of retrieved studies on aspirin's impact on these transcription factors in AS.

Main Results:

  • Aspirin inhibits nuclear factor-kappa B (NF-κB) activation, decreasing pro-inflammatory cytokine release.
  • Aspirin enhances peroxisome proliferator-activated receptors (PPARs) and activating transcription factor 2-alpha (AP-2α) signaling pathways.
  • These modulations contribute to aspirin's anti-inflammatory and plaque-stabilizing effects in AS.
  • Clinical trial data (e.g., ARRIVE, ASPREE) indicate variable cardiovascular outcomes, suggesting dose- and population-dependent effects.

Conclusions:

  • Aspirin effectively modulates critical inflammatory transcription factors (NF-κB, PPARs, AP-2α) in atherosclerosis.
  • These actions provide anti-inflammatory benefits in AS beyond aspirin's established antiplatelet role.
  • Further research is needed to elucidate AP-2α's precise role and develop personalized aspirin combination therapies based on inflammatory profiles.
Abstract

Keywords:
AP‐2αNF‐κBPPARaspirinatherosclerosis

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