Role of GSTM1 in resistance to lung inflammation

Free Radic Biol Med. 2012 Aug 15;53(4):721-9. doi: 10.1016/j.freeradbiomed.2012.05.037. Epub 2012 Jun 6.

Abstract

Lung inflammation resulting from oxidant/antioxidant imbalance is a common feature of many lung diseases. In particular, the role of enzymes regulated by the NF-E2-related factor 2 transcription factor has recently received increased attention. Among these antioxidant genes, glutathione S-transferase Mu 1 (GSTM1) has been most extensively characterized because it has a null polymorphism that is highly prevalent in the population and associated with increased risk of inflammatory lung diseases. Present evidence suggests that GSTM1 acts through interactions with other genes and environmental factors, especially air pollutants. Here, we review GSTM1 gene expression and regulation and summarize the findings from epidemiological, clinical, animal, and in vitro studies on the role played by GSTM1 in lung inflammation. We discuss limitations in the existing knowledge base and future perspectives and evaluate the potential of pharmacologic and genetic manipulation of the GSTM1 gene to modulate pulmonary inflammatory responses.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Air Pollution / adverse effects
  • Animals
  • Antioxidants / therapeutic use
  • Gene Expression
  • Glutathione Transferase / genetics
  • Glutathione Transferase / metabolism
  • Glutathione Transferase / physiology*
  • Humans
  • Oxidative Stress
  • Pneumonia / drug therapy
  • Pneumonia / enzymology*
  • Pneumonia / etiology
  • Sequence Deletion

Substances

  • Antioxidants
  • Glutathione Transferase
  • glutathione S-transferase M1