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Cyclooxygenase Pathway: Prostaglandins and Thromboxanes The cyclooxygenase pathway in eicosanoid biosynthesis is catalyzed by prostaglandin endoperoxide synthase (COX‑1 and COX‑2).​ COX converts arachidonic acid first to prostaglandin G2 (PGG2) and then to prostaglandin H2 (PGH2) via coupled cyclooxygenase and peroxidase activities.​ PGH2 serves as the common precursor for several eicosanoids: prostaglandin E2 (PGE2), PGF2α, prostacyclin (PGI2), and thromboxane A2 (TXA2), each produced by tissue‑specific synthases.​ PGI2 is a vasodilator and inhibitor of platelet aggregation, whereas TXA2 promotes vasoconstriction and platelet aggregation, highlighting the opposing physiological roles within the biosynthesis of eicosanoids network.​ Lipoxygenase Pathway: Leukotrienes, HETEs, and Lipoxins The lipoxygenase pathway of eicosanoid biosynthesis introduces molecular oxygen into arachidonic acid to form hydroperoxy intermediates.​ 5‑lipoxygenase (5‑LOX) converts arachidonic acid into 5‑HPETE, which is then processed into leukotriene A4 (LTA4) and further to leukotrienes such as LTB4, LTC4, LTD4, and LTE4, potent mediators of inflammation and bronchoconstriction.​ 12‑LOX and 15‑LOX yield 12‑HPETE and 15‑HPETE, which are reduced to HETEs and can be further metabolized into lipoxins that generally exert anti‑inflammatory and pro‑resolving effects.​ Leukotrienes are synthesized mainly in leukocytes like neutrophils, eosinophils, and macrophages and play a central role in asthma and allergic inflammation.​ Cytochrome P450 Pathway in Eicosanoid Biosynthesis The cytochrome P450 (CYP) pathway contributes additional branches to the biosynthesis of eicosanoids by epoxidation and hydroxylation of arachidonic acid.​ CYP epoxygenases generate epoxyeicosatrienoic acids (EETs), which modulate vascular tone, endothelial function, and renal sodium handling.​ CYP ω‑hydroxylases produce 20‑HETE and related metabolites that influence vasoconstriction, tubular transport, and blood pressure control.​ Although less emphasized in classic textbooks, CYP‑derived eicosanoids are increasingly recognized as important regulators in cardiovascular and renal physiology.​ Transcellular Biosynthesis of Eicosanoids In many tissues, complete biosynthesis of eicosanoids requires cooperation between different cell types, a process termed transcellular biosynthesis.​ A donor cell possessing primary enzymes (e.g., COX or LOX) generates unstable intermediates such as LTA4 or PGH2 and releases them into the extracellular space.​ Neighboring acceptor cells, which may lack the initial enzyme but express specific downstream synthases, then convert these intermediates into biologically active eicosanoids.​ This transcellular metabolism expands the repertoire of eicosanoids produced within a tissue and allows fine‑tuned local regulation.​ Regulation and Clinical Relevance The biosynthesis of eicosanoids is tightly controlled at several levels, including precursor availability, phospholipase activation, and inducible expression of COX‑2 and certain LOX isoforms during inflammation.​ Nonsteroidal anti‑inflammatory drugs (NSAIDs) inhibit COX enzymes, thereby reducing prostaglandin and thromboxane synthesis and alleviating pain, fever, and inflammation.​ Selective 5‑LOX inhibitors and leukotriene receptor antagonists are used in the management of asthma by limiting leukotriene production or action.​ Dysregulated eicosanoid biosynthesis is implicated in cardiovascular disease, asthma, arthritis, cancer, and metabolic disorders, making these pathways important therapeutic targets.​ On-page SEO suggestions (for your implementation) Update SEO title to: “Biosynthesis of Eicosanoids: Pathways, Enzymes and Functions”

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Angiopoietin-like 4 (Angtpl4)