Kdm6a-CNN1 axis orchestrates epigenetic control of trauma-induced spinal cord microvascular endothelial cell senescence to balance neuroinflammation for improved neurological repair

This study investigates how spinal cord injuries (SCI) cause microvascular endothelial cells to age and become pro-inflammatory. It identifies a protein, Kdm6a (UTX), as a key regulator of this aging process in these cells. The study also shows that removing UTX can protect these cells from aging, reduce inflammation, and improve recovery after SCI. The UTX protein binds to another protein called CNN1, which influences inflammation and neurological repair after a spinal cord injury. Finally, the research suggests that using senolytic drugs to eliminate aged cells can improve the regenerative environment and enhance functional repair after SCI.

• 1
  Spinal cord injury (SCI) induces senescence in spinal cord microvascular endothelial cells (SCMECs).
• 2
  Upregulation of UTX induces senescence in SCMECs, leading to an amplified release of pro-inflammatory factors.
• 3
  Targeting the UTX-CNN1 epigenetic axis to prevent trauma-induced SCMECs senescence holds the potential to inhibit SASP secretion, alleviate neuroinflammation, and provide a novel treatment strategy for SCI repair.