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The **pro-inflammatory lipid mediator pathway** encompasses the enzymatic generation of lipid signaling molecules—primarily prostaglandins, leukotrienes, and other eicosanoids—from polyunsaturated fatty acids such as arachidonic acid[1][2][3]. These mediators play key roles in orchestrating the acute inflammatory response: they regulate vascular tone and permeability, promote leukocyte (especially neutrophil) recruitment, and modulate immune cell activity. Upon tissue injury or infection, phospholipase-mediated release of arachidonic acid is followed by conversion via cyclooxygenase (COX) and lipoxygenase (LOX) enzymes into bioactive lipid mediators. Drugs such as NSAIDs and leukotriene antagonists target components of these pathways to control inflammation[1][2][3]. Disruption or chronic overactivation is implicated in a wide range of diseases, including autoimmune disorders, cardiovascular diseases, cancer, and neurodegeneration. Importantly, a counter-regulatory class of pro-resolving lipid mediators also arises from these metabolic routes, highlighting the dual and dynamic nature of lipid signaling in inflammation and resolution[1][3][5].
Inhibition of prostaglandin synthesis (NSAIDs inhibit cyclooxygenases COX-1 and COX-2); Blockade of leukotriene receptors; Modulation of arachidonic acid metabolism
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