Eicosanoid pathway modulation via omega-3 fatty acids

Eicosanoid pathway modulation via omega‑3 fatty acids" does not refer to a single molecular target but rather describes the process by which dietary or supplemental omega‑3 polyunsaturated fatty acids—primarily eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—alter the metabolism of arachidonic acid through the eicosanoid biosynthetic pathways. Normally, arachidonic acid is converted by cyclooxygenases and lipoxygenases into potent pro-inflammatory mediators called eicosanoids. When cell membranes are enriched with EPA/DHA through diet or supplementation, these omega‑3s compete with arachidonic acid for enzymatic conversion. This competition results in decreased production of highly inflammatory prostaglandins and leukotrienes from arachidonic acid while increasing the formation of less inflammatory or even anti-inflammatory/pro-resolving lipid mediators such as resolvins and protectins from EPA/DHA. This shift underlies many observed benefits on inflammation resolution, cardiovascular health, immune function regulation, and possibly neuroprotection. However, because this entry refers to a broad metabolic process rather than an individual protein target like an enzyme or receptor—and encompasses multiple molecules—it is not considered a canonical therapeutic target itself but rather describes a mechanism that can be therapeutically exploited using drugs/supplements containing omega‑3 fatty acids. This entry is marked as incorrect for use as a canonical drug target because it refers to an entire biochemical pathway modulated by nutrient intake—not an individual molecular entity such as an enzyme ("cyclooxygenase"), receptor ("prostaglandin receptor"), transporter etc., which are standard drug targets.

Other names

Omega-3 fatty acid-mediated eicosanoid modulationOmega-3 PUFA effects on eicosanoid synthesisModulation of eicosanoids by EPA/DHA

Competitive inhibition of arachidonic acid metabolism by cyclooxygenase and lipoxygenase enzymes; Reduction in pro-inflammatory eicosanoid production; increase in less inflammatory or pro-resolving lipid mediators such as resolvins and protectins derived from EPA/DHA instead of arachidonic acid