S100A8 aggravates sepsis-associated encephalopathy by promoting PFKFB3-dependent glycolysis and microglial neuroinflammation

Key Points

• Sepsis-associated encephalopathy is aggravated by s100a8, increasing neuroinflammation and affecting brain function.
• Findings reveal that s100a8 promotes pfkfb3-dependent glycolysis, which plays a pivotal role in microglial activation.
• The analysis utilized cellular models of neuroinflammation to investigate mechanisms of s100a8 action.
• These insights may help develop new treatments for sepsis-related brain complications, though clinical application requires further validation.