Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, inhibit COX isforms to achieve antipyretic, analgesic, and anti-inflammatory actions through blocking PGs biosynthesis (Funk, 2001).
Prostaglandins (PGs), a group of key lipid mediators, are involved in numerous physiological and pathological processes including inflammation and cardiovascular homeostasis. Each PG acts on its specific and distinct cell surface G protein-coupled receptors (GPCRs) or peroxisome proliferator-activated receptors (PPARs). Prostaglandin F2αreceptor (FP) is required for female reproductive function such as luteolysis and parturition. It has recently been implicated in blood pressure regulation, atherosclerosis and other inflammation-related disorders. The emerging role of FP in cardiovascular diseases is highlighted and potential therapeutic translation is discussed in the current review.
Prostaglandins (PGs), a group of key lipid mediators, are involved in numerous physiological and pathological processes including inflammation and cardiovascular homeostasis. Each PG acts on its specific and distinct cell surface G protein-coupled receptors (GPCRs) or peroxisome proliferator-activated receptors (PPARs). Prostaglandin F2αreceptor (FP) is required for female reproductive function such as luteolysis and parturition. It has recently been implicated in blood pressure regulation, atherosclerosis and other inflammation-related disorders. The emerging role of FP in cardiovascular diseases is highlighted and potential therapeutic translation is discussed in the current review.
No comments:
Post a Comment