prostaglandinmediated

Prostaglandin-mediated refers to the biological effects driven by prostaglandins, a family of lipid mediators derived from arachidonic acid. In most tissues, phospholipase A2 releases arachidonic acid, which is converted by cyclooxygenases COX-1 and COX-2 into the common precursor PGH2. Specific synthases then convert PGH2 into the individual prostaglandins—PGE2, PGD2, PGF2alpha, and prostacyclin (PGI2)—as well as thromboxane A2, among others. Prostaglandins typically act locally in autocrine or paracrine fashion and signal through distinct G protein–coupled receptors. Receptor subtypes include EP1-4 for PGE2, FP for PGF2alpha, DP1/DP2 for PGD2, IP for PGI2, and TP for thromboxane. Receptor coupling to G proteins modulates cyclic AMP, calcium, and IP3/DAG pathways, producing diverse responses such as changes in vascular tone, platelet function, and nociception.

Physiological roles are broad and context-dependent. PGE2 modulates inflammation, fever, and pain; PGI2 and PGE2 influence vascular dilation, renal function, and platelet dynamics; PGD2 participates in sleep regulation and allergic responses; PGF2alpha affects uterine contraction and reproductive processes. In the central nervous system, prostaglandins contribute to fever and pain sensitization. Pathologically, prostaglandin-mediated signaling can contribute to inflammatory diseases, migraine, cancer progression, and tissue injury, often amplified by cyclooxygenase-2 during inflammation.

Therapeutically, prostaglandin pathways are targeted by nonsteroidal anti-inflammatory drugs that inhibit COX enzymes, reducing prostaglandin synthesis and alleviating pain and inflammation. Prostanoid receptor modulators and prostaglandin analogs are used clinically for specific indications, such as misoprostol (PGE1) for gastric protection, dinoprostone (PGE2) for cervical ripening, latanoprost (a PGF2alpha analog) for glaucoma, and epoprostenol (a PGI2 analog) for pulmonary arterial hypertension.