Targeting PGE2 receptor subtypes rather than cyclooxygenases: a bridge over troubled water?

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Prostaglandins (PG) are synthesized by the sequential action of phosholipases, cyclooxygenases (COX)-1 and COX-2, and specific terminal synthases, and exert their diverse biological effects through several membrane receptors. In particular, PGE2 is involved in many normal and pathological pathways that are mediated by four different E prostanoid receptors (EP1-4). Selective COX-2 inhibitors (Coxibs) have analgesic and antipyretic effects that are indistinguishable from those of nonsteroidal anti-inflammatory drugs (NSAIDs), but some possess hazardous cardiovascular side effects. Recent results indicate that EP1 and EP4 antagonists might prove useful for inhibiting the unwanted actions of COX-2. Has the time come for research to examine earnestly the selective antagonism of EP subtypes rather than further the development of direct COX-2 inhibitors?
Original languageEnglish
Pages (from-to)68-68-73, 58
JournalMolecular Interventions
Volume6
DOIs
Publication statusPublished - 2006

Keywords

  • Animals
  • Arachidonic Acid
  • Cyclooxygenase 1
  • Dinoprostone
  • Gene Expression Regulation
  • Humans
  • Membrane Proteins
  • Mice
  • Mice, Knockout
  • Models, Biological
  • Organ Specificity
  • Prostaglandin-Endoperoxide Synthases
  • Receptors, Prostaglandin E
  • Signal Transduction
  • Tissue Distribution
  • Water

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