S100A11 regulates microglial inflammatory response in neuropathic pain via H3K27ac-TFEB-mitochondrial autophagy axis - PubMed
a day ago
- #Autophagy
- #Neuropathic pain
- #Microglia
- S100A11 is significantly upregulated in activated spinal microglia in neuropathic pain (NP).
- Microglia-targeted S100A11 knockdown alleviates mechanical/thermal hyperalgesia and reduces spinal synaptic damage in NP mice.
- S100A11 silencing suppresses microglial pyroptosis and proinflammatory cytokine release while enhancing autophagic flux.
- S100A11 depletion promotes TFEB nuclear translocation and increases H3K27ac at autophagy gene promoters.
- H3K27ac-mediated chromatin relaxation facilitates TFEB binding, activating autophagy machinery and restoring microglial homeostasis.
- The study identifies a novel S100A11-TFEB-H3K27ac-autophagy regulatory axis in microglial dysfunction during NP.