Lysoglycerophospholipids in chronic inflammatory disorders: the PLA(2)/LPC and ATX/LPA axes

Biochim Biophys Acta. 2013 Jan;1831(1):42-60. doi: 10.1016/j.bbalip.2012.07.019. Epub 2012 Jul 31.

Abstract

Lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA), the most prominent lysoglycerophospholipids, are emerging as a novel class of inflammatory lipids, joining thromboxanes, leukotrienes and prostaglandins with which they share metabolic pathways and regulatory mechanisms. Enzymes that participate in LPC and LPA metabolism, such as the phospholipase A(2) superfamily (PLA(2)) and autotaxin (ATX, ENPP2), play central roles in regulating LPC and LPA levels and consequently their actions. LPC/LPA biosynthetic pathways will be briefly presented and LPC/LPA signaling properties and their possible functions in the regulation of the immune system and chronic inflammation will be reviewed. Furthermore, implications of exacerbated LPC and/or LPA signaling in the context of chronic inflammatory diseases, namely rheumatoid arthritis, multiple sclerosis, pulmonary fibrosis and hepatitis, will be discussed. This article is part of a Special Issue entitled Advances in Lysophospholipid Research.

Publication types

  • Review

MeSH terms

  • Animals
  • Chronic Disease
  • Humans
  • Inflammation / enzymology*
  • Inflammation / pathology
  • Lysophosphatidylcholines / metabolism*
  • Lysophospholipids / metabolism*
  • Phospholipases A2 / metabolism*
  • Phosphoric Diester Hydrolases / metabolism*
  • Signal Transduction

Substances

  • Lysophosphatidylcholines
  • Lysophospholipids
  • Phospholipases A2
  • Phosphoric Diester Hydrolases
  • alkylglycerophosphoethanolamine phosphodiesterase
  • lysophosphatidic acid