Prostaglandins and leukotrienes: advances in eicosanoid biology

Science. 2001 Nov 30;294(5548):1871-5. doi: 10.1126/science.294.5548.1871.

Abstract

Prostaglandins and leukotrienes are potent eicosanoid lipid mediators derived from phospholipase-released arachidonic acid that are involved in numerous homeostatic biological functions and inflammation. They are generated by cyclooxygenase isozymes and 5-lipoxygenase, respectively, and their biosynthesis and actions are blocked by clinically relevant nonsteroidal anti-inflammatory drugs, the newer generation coxibs (selective inhibitors of cyclooxygenase-2), and leukotriene modifiers. The prime mode of prostaglandin and leukotriene action is through specific G protein-coupled receptors, many of which have been cloned recently, thus enabling specific receptor agonist and antagonist development. Important insights into the mechanisms of inflammatory responses, pain, and fever have been gleaned from our current understanding of eicosanoid biology.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Fever / drug therapy
  • Fever / metabolism
  • Humans
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Leukotriene Antagonists
  • Leukotrienes / agonists
  • Leukotrienes / biosynthesis
  • Leukotrienes / metabolism*
  • Pain / drug therapy
  • Pain / metabolism
  • Prostaglandin Antagonists / pharmacology
  • Prostaglandin Antagonists / therapeutic use
  • Prostaglandins / agonists
  • Prostaglandins / biosynthesis
  • Prostaglandins / metabolism*
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Receptors, Leukotriene / metabolism
  • Transcription Factors / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Leukotriene Antagonists
  • Leukotrienes
  • Prostaglandin Antagonists
  • Prostaglandins
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Leukotriene
  • Transcription Factors