Sodium Butyrate Promotes Enteric Glial Cells Neurogenesis by Inhibiting Kdm2a and Inducing Klf4 Expression

In brief

This study investigates sodium butyrate as a therapeutic agent for Hirschsprung disease by examining its effects on enteric glial cells. The research identifies specific molecular mechanisms—inhibition of Kdm2a and induction of Klf4—through which sodium butyrate promotes neurogenesis in the enteric nervous system, offering potential new treatment strategies for this congenital disorder.

• Sodium butyrate (NaB) promotes neurogenesis in enteric glial cells, offering a potential therapeutic mechanism for Hirschsprung disease.
• NaB inhibits Kdm2a expression, a histone demethylase that may suppress neurogenic pathways in the enteric nervous system.
• NaB induces Klf4 expression, a transcription factor critical for glial cell differentiation and enteric neuron development.
• Targeting epigenetic regulators like Kdm2a may represent a novel approach to restore enteric nervous system function in HSCR.

Written by the GCMD Library team from the article.