NEAT1 and Sepsis: In the cecal ligation and puncture (CLP) rat model, blood-brain barrier damage and increased reactive oxygen species (ROS) levels promote ferroptosis, during which the expression of serum exosomal NEAT1 is upregulated, potentially regulating miR-9-5p/TFRC and GOT1 axis through a competing endogenous RNA mechanism to promote neuronal ferroptosis in rats, thus exacerbating sepsis-associated encephalopathy 140.