Highlights

• This study confirmed the methylation of TRAF2 (a crucial cytoplasmic protein) by SMYD2 in the NF-κB signaling pathway.
• SMYD2-mediated methylation of TRAF2 prolongs NF-κB signaling by inhibiting TRAF2 proteolysis and enhancing its activity.
• By uncovering the role of SMYD2-mediated TRAF2 methylation in promoting NF-κB activation, this study offers potential therapeutic targets for inflammation diseases.

Summary

This research focuses on TRAF2, a critical factor in NF-κB activation. Scientists have investigated the impact of SMYD2-mediated methylation on TRAF2 and its role in the NF-κB signaling pathways in inflammatory diseases. The results confirm that SMYD2 methylates TRAF2, leading to prolonged NF-κB signaling transduction by inhibiting TRAF2 proteolysis and enhancing activity.

The research also explores the effects of SMYD2 in acute and chronic inflammation mouse models, showing varying degrees of mitigation upon eliminating SMYD2. Additionally, lysine-specific demethylase LSD1 is capable of counteracting TRAF2 methylation induced by SMYD2. This observation offers potential therapeutic targets for inflammatory diseases.

In conclusion, SMYD2 overexpression promotes NF-κB pathways in inflammatory diseases. The insight into the regulation of NF-κB signaling provides a deeper understanding of the molecular mechanisms underlying inflammatory responses.

Wu et al., “SMYD2‐mediated TRAF2 methylation promotes the NF‐κB signaling pathways in inflammatory diseases,” Clinical & Translational Med, vol. 11, no. 11, p. e591, Nov. 2021, doi: .