COXensüümed

COXensüümed, also known as cyclooxygenases, are a family of enzymes that play a crucial role in the human body. They are primarily responsible for catalyzing the conversion of arachidonic acid into prostaglandins and thromboxanes, which are signaling molecules involved in a wide range of physiological processes. There are two main isoforms of COX enzymes: COX-1 and COX-2.

COX-1 is constitutively expressed, meaning it is produced continuously in many tissues, including the stomach, kidneys, and platelets. It is involved in maintaining normal physiological functions such as protecting the stomach lining from acid, regulating kidney blood flow, and facilitating platelet aggregation.

COX-2, on the other hand, is typically induced, meaning its expression is upregulated in response to inflammatory stimuli, such as injury or infection. COX-2 is predominantly found at sites of inflammation and is a key mediator of pain, fever, and swelling.

The inhibition of COX enzymes is the mechanism of action for a widely used class of drugs known as nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen, and naproxen. By blocking COX activity, NSAIDs reduce the production of prostaglandins and thromboxanes, thereby alleviating pain and inflammation. However, inhibiting COX-1 can lead to gastrointestinal side effects, while inhibiting COX-2 selectively can reduce inflammation with fewer gastrointestinal issues, though with potential cardiovascular risks. Understanding the distinct roles of COX-1 and COX-2 is vital for developing targeted therapies.