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Role of GSTM1 in Resistance for Lung Inflammation
Citation:
Wu, W., D. Peden, AND D. Diaz-Sanchez. Role of GSTM1 in Resistance for Lung Inflammation. Free Radical Biology and Medicine. Elsevier Science Ltd, New York, NY, 53(4):721-9, (2012).
Impact/Purpose:
Chronic inflammation is a feature of many common lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD) [1,2]. There is now substantial evidence that oxidative stress plays an important role in the injurious and inflammatory responses central to many lung diseases. As a part of endogenous metabolism, as well as in response to challenge by inhaled environmental agents, the lung continuously generates reactive forms of oxygen, as well as free radical species [3].
Description:
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 (Nrf2) transcription factor has recently received increased attention. Among these antioxidant genes, the glutathione S-transferase mu 1 (GSTM1) has been most extensively characterized since it has a null polymorphism which is highly prevalent in the population and associated with increased risk of inflammatory lung disease. Present evidence suggests that GSTMl acts through interactions with other genes and environmental factors, especially air pollutants. Here, we review GSTMl 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 GSTMl gene to modulate pulmonary inflammatory responses.
