There are two isozymes of PTGS: a constitutive PTGS1 and an inducible PTGS2, which differ in their regulation of expression and tissue distribution. PTGS1, which regulates angiogenesis in endothelial cells, and is inhibited by nonsteroidal anti-inflammatory drugs such as aspirin. Recent research has shown that the inhibition of COX-1 is the main reason why aspirin is effective at reducing cardiac events (as opposed to aspirin's anti-platelet aggregation effects).
PTGS1 is thought to be involved in cell-cell signaling and maintaining tissue homeostasis. Alternative splicing of this gene generates two transcript variants called COX-1 and COX-3. The expression of these two transcripts is differentially regulated by relevant cytokines and growth factors.