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The arachidonic acid metabolic pathway encompasses the release of arachidonic acid (AA) from cell membrane phospholipids, typically triggered by phospholipase A2, and its subsequent conversion by three principal enzymatic routes: cyclooxygenase (COX) to prostaglandins and thromboxanes; lipoxygenase (LOX) to leukotrienes and lipoxins; and cytochrome P450 (CYP) to epoxyeicosatrienoic acids and hydroxyeicosatetraenoic acids. These metabolites orchestrate diverse biological effects, including mediation of inflammation, immune responses, vascular tone, pain, and tissue homeostasis. Dysregulation of this pathway is implicated in inflammatory diseases, cardiovascular and metabolic disorders, neurodegeneration, and cancer. Numerous drugs target enzymes within this pathway to control inflammation and related conditions—making it a nexus of research and clinical intervention. However, as a pathway, it should not be classified as a single molecular target for structured drug or biomarker databases; its therapeutic significance lies in the individual molecular components, each with distinct biological roles and pharmacological relevance.
Enzyme inhibition (block conversion of AA to prostaglandins, thromboxanes, or leukotrienes); Receptor antagonism (block eicosanoid receptors); Modulation of substrate availability (inhibit AA release)
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