signalprostaglandin

Signalprostaglandin is not a standard term in the scientific literature, but it can be used as a descriptor for the class of prostaglandin-mediated signaling molecules that regulate numerous physiological processes. Prostaglandins are lipid mediators derived from arachidonic acid through cyclooxygenase enzymes and act as autocrine and paracrine signals in diverse tissues. They are synthesized on demand rather than stored and participate in rapid, localized responses to cellular stress, injury, and infection.

Biosynthesis and signaling occur via a two-step process. Phospholipase A2 releases arachidonic acid from membrane phospholipids, and cyclooxygenases convert it to the unstable intermediate prostaglandin H2 (PGH2). Specific synthases then generate distinct prostaglandins, including PGE2, PGD2, PGF2α, prostacyclin (PGI2), and thromboxane A2 (TXA2). Each prostaglandin binds to corresponding G protein–coupled receptors (for example, PGE2 to EP1–EP4, PGI2 to IP, TXA2 to TP, PGD2 to DP1/DP2). Receptor engagement triggers intracellular signaling cascades such as increased or decreased cAMP, phospholipase C activation, inositol trisphosphate/calcium flux, and protein kinase activity, shaping cellular responses.

Physiological roles of signalprostaglandins are broad. They regulate inflammation, pain, and fever, and influence vascular tone, platelet function, gastric protection, renal function, and smooth muscle activity. Clinically, nonsteroidal anti-inflammatory drugs reduce prostaglandin synthesis to alleviate pain and inflammation but can cause gastric irritation or cardiovascular effects by altering the balance of prostaglandin signaling.

In summary, signalprostaglandin describes prostaglandin-based signaling mediators, a well-established concept under a nonstandard term, central to inflammatory and homeostatic processes across tissues.