aspirintriggered

Aspirintriggered refers to a set of biochemical mediators and inflammatory responses that arise when aspirin modulates the activity of cyclooxygenase enzymes, particularly COX-2. The term is commonly used to describe aspirin-triggered lipoxins and related pro-resolving mediators generated through aspirin’s acetylation of COX-2, which redirects arachidonic acid metabolism toward 15-epi-lipoxins and other epimeric mediators.

Mechanism and mediators: When aspirin acetylates COX-2, it inhibits the production of certain pro-inflammatory prostaglandins and enables the formation of 15R-hydroxyeicosatetraenoic acid, which 5-LOX can convert into 15-epi-lipoxin A4 (15-epi-LXA4). Similar acetylation-driven pathways can generate aspirin-triggered resolvins and related species from EPA and DHA. These aspirin-triggered mediators often have enhanced stability or distinct receptor interactions compared with classical counterparts and are associated with anti-inflammatory and pro-resolving actions, such as reduced neutrophil recruitment and enhanced clearance of inflammatory cells.

Scope and significance: The aspirintriggered axis has been observed in various cell types, including leukocytes and endothelial cells, and can occur during regular aspirin therapy in humans. It is studied for its potential contribution to aspirin’s beneficial effects in cardiovascular disease and inflammatory conditions, beyond its primary antiplatelet action.

History and context: The concept emerged from research in the 1990s identifying aspirin-triggered lipoxins and recognizing aspirin’s unique ability to steer lipid mediator biosynthesis toward pro-resolving pathways.