Eicosanoid metabolism pathway (Eicosanoid pathway)

The cell membrane phospholipids and endogenous eicosanoid synthesis pathways represent a complex network of biochemical reactions that convert membrane-derived fatty acids into potent lipid mediators (StatPearls: Eicosanoids). The process typically begins with the activation of phospholipase A2 (PLA2), which releases arachidonic acid from the cell membrane (PubMed: PMID 29107073). Arachidonic acid is then metabolized via three primary enzymatic routes: the cyclooxygenase (COX) pathway leading to prostaglandins and thromboxanes, the lipoxygenase (LOX) pathway leading to leukotrienes, and the cytochrome P450 pathway (NIH: Eicosanoid Signaling). These eicosanoids act as local hormones, regulating diverse physiological processes including inflammation, fever, blood pressure, and platelet aggregation. Dysregulation of this pathway is a hallmark of many chronic inflammatory diseases, such as rheumatoid arthritis and asthma (PubMed: PMID 30503903). Consequently, this pathway is a major focus of pharmacology, with widely used drugs like nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids acting to suppress the production of pro-inflammatory eicosanoids (StatPearls: NSAIDs). Therapeutic intervention can also involve blocking specific eicosanoid receptors, such as the cysteinyl leukotriene receptors in asthma management (PubMed: PMID 25172511).

Other names

Arachidonic acid cascadeEicosanoid metabolism pathwayProstaglandin and leukotriene synthesis pathwaysCell membrane phospholipids and endogenous eicosanoid synthesis pathways

Drugs targeting this pathway primarily act by inhibiting key enzymes such as Phospholipase A2 (via lipocortin induction), Cyclooxygenase-1 (COX-1), Cyclooxygenase-2 (COX-2), and 5-Lipoxygenase (5-LOX), or by antagonizing downstream G protein-coupled receptors like the cysteinyl leukotriene receptors (StatPearls: NSAIDs; PubMed: PMID 25172511).