PKM2 accelerated the progression of chronic fatigue syndrome via promoting the H4K12la/ NF-κB induced neuroinflammation and mitochondrial damage.

ABSTRACT: This study aims to explore the effects and potential mechanisms of PKM2-mediated neuroinflammation leading to mitochondrial damage and its role in the progression of chronic fatigue syndrome (CFS). Bioinformatics methods were applied to predict and analyze PKM2 and downstream signaling factors. In vivo experiments were conducted with mice divided into four groups after different treatments: control group, model group, Model + PKM2-OE group, and Model + PKM2-KD group. Morris water maze and field tests were used to assess cognitive function, grip strength, and rotation tests to evaluate physical strength. HE and Nissl staining were used to observe cellular conditions in the CA1 region of the hippocampus. Immunohistochemistry was used to detect PKM2 levels in the CA1 region. Western blot was

SUBMITTER: Sun M 

PROVIDER: S-EPMC11953386 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature