Prostaglandin synthesis pathway enzyme

Prostaglandin synthesis pathway enzymes are a group of enzymes responsible for the conversion of arachidonic acid into various prostaglandins, crucial lipid mediators involved in inflammation, pain, vascular function, reproduction, and homeostasis. The pathway begins with phospholipase A₂ releasing arachidonic acid from membrane phospholipids, which is then converted by cyclooxygenases (COX-1/COX-2, also prostaglandin G/H synthases) to the intermediate prostaglandin H₂ (PGH₂). Specific synthases and isomerases such as prostaglandin E synthase (PGES, including mPGES-1, mPGES-2, cPGES), prostaglandin D synthase (PGDS), prostacyclin synthase (PGIS), and thromboxane synthase subsequently produce the biologically active prostanoids (PGE₂, PGD₂, PGI₂, TXA₂, etc.). Many of these enzymes, especially mPGES-1 and COX-2, are inducible in disease contexts and represent validated therapeutic targets for inflammatory conditions, pain, and cancer. Their inhibition forms the basis for several drug classes including NSAIDs and experimental prostaglandin synthase inhibitors. Depending on the context, these enzymes may exhibit tissue- and isoform-specific functions and expression patterns, influencing both therapeutic efficacy and safety. For structured database use, the pathway should be subdivided by enzyme (e.g., "Prostaglandin E synthase", "Cyclooxygenase-2") rather than using "Prostaglandin synthesis pathway enzyme" as a collective term.

Other names

PGESmPGES-1mPGES-2cPGEScyclooxygenase (COX-1/COX-2)prostaglandin synthasePGD synthasePGI synthasethromboxane synthase

Enzyme inhibition (e.g., NSAIDs inhibit COX enzymes to block prostaglandin production); Isoform-specific inhibition (selective PGES inhibitors block PGE₂ production without affecting others); Downregulation of mPGES-1 (by glucocorticoids)