Inflammatory mediators and NSAID effects

When tissue is damaged or infected, the body releases signaling molecules called prostaglandins that drive inflammation—a process centrally governed by an enzyme called cyclooxygenase-2, or COX-2. Non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and naproxen, along with more targeted agents such as celecoxib and rofecoxib, work largely by blocking this enzyme, reducing pain and swelling but also, unexpectedly, lowering rates of certain cancers like colorectal cancer—an observation that opened a serious line of inquiry into whether these drugs could be used deliberately to prevent malignancy. The difficulty is that suppressing COX-2 also disrupts the balance of molecules that protect blood vessels and the stomach lining, which is why some COX-2 selective drugs were withdrawn after they were linked to elevated cardiovascular risk. Researchers are now working to understand precisely how prostaglandin E2 shapes immune responses within tumors, and whether safer compounds or dosing strategies could preserve the chemopreventive benefit without the cardiovascular and gastrointestinal costs.

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Keywords

Cyclooxygenase-2 InhibitorsInflammationCancerProstaglandinsNSAIDsCardiovascular Risk