COX-2 in cardiovascular disease.
نویسندگان
چکیده
Prostanoids are a large family of lipid mediators derived from the arachidonic acid metabolites of the cyclooxygenase (COX) enzymes. Therapeutically, COX is the target of the nonsteroid antiinflammatory drugs (NSAIDs), a chemically diverse group that includes ibuprofen, naproxen, and diclofenac, among dozens of others. Inhibition of prostanoid production by traditional NSAIDs accounts for all their major therapeutic effects, such as the dampening down of inflammation and the reduction of fever, and their potentially severe adverse side effects, most commonly within the gastrointestinal tract.1,2
منابع مشابه
The cardiovascular pharmacology of COX-2 inhibition.
Selective inhibitors of cyclooxygenase (COX)-2, the coxibs, were developed to inhibit inflammatory prostaglandins derived from COX-2, while sparing gastroprotective prostaglandins primarily formed by COX-1. However, COX-2-derived prostaglandins mediate not only pain and inflammation but also affect vascular function, the regulation of hemostasis/ thrombosis, and blood pressure control. All coxi...
متن کاملCyclooxygenase-2 inhibition increases lipopolysaccharide-induced atherosclerosis in mice.
AIMS The risk of adverse cardiovascular events in humans is increased with chronic use of cyclooxygenase-2 (COX-2) inhibitors. However, the role of COX-2 in animal models of cardiovascular disease has been controversial. In humans and animal models, cardiovascular disease is increased by bacterial infection of the supporting tissue of the teeth, a condition known as periodontal disease. Periodo...
متن کاملCommentary. COX-2-derived prostacyclin confers atheroprotection on female mice.
Female gender affords relative protection from cardiovascular disease until the menopause. We report that estrogen acts on estrogen receptor subtype alpha to up-regulate the production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-2). This mechanism restrained both oxidant stress and platelet activation that contribute to atherogenesis in female mice. Deletion o...
متن کاملCardiovascular effects of common analgesics.
The clycoxygenase (COX) enzyme forms locally active prostaglandins responsible for producing inflammation and pain. Classical non-steroidal anti-inflammatory drugs (NSAID) inhibit the COX-2 enzyme that produces inflammatory prostaglandins as well as the COX-1 enzyme that produces gastric mucosa protecting prostaglandins. By specifically inhibiting only the COX-2 enzyme, coxibs thus reduce pain ...
متن کامل[Nonsteroidal anti-inflammatory drugs: cardiovascular, cerebrovascular and renal effects].
The nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most often prescribed drugs in the world. This heterogeneous class of drugs includes aspirin and several other selective or non-selective cyclooxygenase (COX) inhibitors. The non-selective NSAIDs are the oldest ones and are called traditional or conventional NSAIDs. The selective NSAIDs are called COX-2 inhibitors. In recent years,...
متن کاملCardiovascular Effects of COX-2 Inhibitors: A Review of the Literature
When cyclooxygenase-2 (COX-2) inhibitors (coxibs) came on the market, they were expected to provide a treatment alternative to nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) for patients who were at risk for gastrointestinal (GI) complications. For more than five years, coxibs have been prescribed to millions of patients for the treatment of arthritis, acute pain, Alzheimer’s diseas...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Arteriosclerosis, thrombosis, and vascular biology
دوره 26 5 شماره
صفحات -
تاریخ انتشار 2006