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Hepatic steatosis is the main characteristic of some liver metabolism diseases. However, unclear molecular mechanism of hepatic steatosis impedes the therapy of this hepatic steatosis. Glutathione-S-transferase mu 2 ( GSTM2 ), as a member of phase II drug metabolizing enzymes (DMEs), regulates cellular antioxidant and detoxificant.  GSTM2  was highly up-regulated in hepatic steatosis tissues and high-fat diet (HFD) fed mice. Loss-of-function  GSTM2  mouse model demonstrated that  GSTM2  protected mice from excess fat accumulation. Mechanistically,  GSTM2  interacted with ASK1 and suppressed its phosphorylation and the activation of subsequent downstream p38-JNK signalling. Moreover,  GSTM2  overexpression in the liver effectively ameliorated hepatic lipid accumulation. Therefore, we identified  GSTM2  as an important negative regulator in progression of hepatic steatosis via both its detoxification/antioxidant and inhibition of ASK1-p38/JNK signalling. This study showed potential therapeutic function of the DME in progression of hepatic steatosis.

Glutathione S-transferase Mu 2 inhibits hepatic steatosis via ASK1 suppression