Inflammatory mediators and NSAID effects

When cells are damaged or infected, enzymes called cyclooxygenases convert fatty acids into prostaglandins, small signaling molecules that drive inflammation, fever, and pain. Non-steroidal anti-inflammatory drugs like aspirin, naproxen, and the more targeted COX-2 inhibitors block this pathway, which is why they relieve symptoms — but also why long-term use can disrupt the protective lining of the stomach or, in the case of some COX-2 inhibitors, tip the cardiovascular system toward clotting. A striking observation complicates the picture: people who take these drugs regularly appear to develop colorectal cancer at lower rates, pointing to a role for prostaglandin E2 in suppressing immune surveillance and fueling tumor growth. Researchers are now working to understand whether safer dosing strategies or tissue-selective compounds could preserve that chemopreventive benefit without the cardiovascular and gastrointestinal costs that led to the withdrawal of drugs like rofecoxib.

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Keywords

Cyclooxygenase-2 InhibitorsInflammationCancerProstaglandinsNSAIDsCardiovascular Risk