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

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.