KANK4 Regulates CXCL16 Glycosylation Through TMEM260 to Modulate Microglial Activation in Sepsis-associated Encephalopathy - PubMed
6 hours ago
- #Microglial Activation
- #Neuroinflammation
- #Sepsis-associated Encephalopathy
- KANK4 expression is downregulated in the hippocampus of SAE mice and LPS-induced microglial cells.
- Downregulation of KANK4 correlates with microglial overactivation and increased pro-inflammatory cytokines (IL-1β, IL-6, TNF-α).
- Hippocampal overexpression of KANK4 improves cognitive performance in SAE mice and alleviates neuronal damage.
- KANK4 binds to TMEM260 mRNA's 3'UTR to enhance its stability, inhibiting CXCL16 glycosylation and expression.
- TMEM260 overexpression reduces CXCL16 levels and neuroinflammation, while CXCL16 overexpression reverses TMEM260's neuroprotective effects.
- The KANK4-TMEM260-CXCL16 axis is crucial for regulating microglial activation, offering a new therapeutic target for SAE.