Key result
Aspirin modulates atherosclerotic inflammation by inhibiting NF-κB and enhancing PPAR signaling despite variable cardiovascular outcomes.
Why the study?
Atherosclerosis involves chronic inflammation mediated by transcription factors, and beyond its antiplatelet role, aspirin may exert anti-inflammatory effects influencing these molecular pathways.
Does aspirin modulate transcription factors related to inflammation in atherosclerosis?
Systematic Review
Does aspirin modulate transcription factors related to inflammation in atherosclerosis?
Aspirin exerts anti-inflammatory and plaque-stabilizing effects in atherosclerosis by modulating key transcription factors like NF-κB, PPARs, and AP-2α, offering potential benefits beyond platelet inhibition.
Answers are grounded in this paper and cite their sources.
May warrant consideration of aspirin's pleiotropic effects in CAD management; extends evidence beyond antiplatelet activity.
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.
No takes yet. Share an insight, caveat, or question.
Aghaei et al. (2026) conducted a systematic review in Atherosclerosis. Aspirin was evaluated on Modulatory effects on transcription factors (NF-κB, PPARs, and AP-2α) in atherosclerosis. Aspirin modulates key inflammatory transcription factors in atherosclerosis by inhibiting NF-κB and enhancing PPAR and AP-2α signaling, though clinical trials show variable cardiovascular outcomes.
Synapse has enriched 10 related papers. Consider them for comparative context: