Increased TSPO alleviates neuropathic pain by preventing pyroptosis via the AMPK-PGC-1α pathway.

ABSTRACT: Neuropathic pain poses a significant clinical challenge, largely due to the incomplete understanding of its molecular mechanisms, particularly the role of mitochondrial dysfunction. Bioinformatics analysis revealed that pyroptosis and inflammatory responses induced by spared nerve injury (SNI) in the spinal dorsal horn play a critical role in the initiation and persistence of neuropathic pain. Among the factors involved, TSPO (translocator protein) emerged as a key regulator. Our experimental findings showed that TSPO expression was upregulated during neuropathic pain, accompanied by mitochondrial dysfunction, specifically manifested as impaired mitochondrial biogenesis, disrupted mitochondrial dynamics (including insufficient expression of mitochondrial biogenesis and fusion-related prote

SUBMITTER: Li B 

PROVIDER: S-EPMC11771075 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature