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We read with great interest the recent Gut article by Yang and colleagues showing that SMYD2 acts as a hepatoprotective regulator during hepatic ischaemia/reperfusion (I/R) injury. In paired human hepatectomy samples, higher post-I/R SMYD2 expression was associated with better postoperative liver function. Mechanistically, the authors identify SMYD2-mediated STAT1 methylation at lysine 175 as a brake on STAT1 phosphorylation and nuclear translocation, thereby limiting inflammatory and apoptotic signalling in hepatocytes.1