Molecular regulatory mechanism of the SIRT2/NF-κB p65 signaling pathway in ferroptosis-promoted spinal cord injury repair.

ABSTRACT:

Background

Spinal cord injury (SCI) is a debilitating neurological condition that often results in long-term disability and functional impairment. Recent studies have identified ferroptosis as a significant pathological mechanism in SCI. SIRT2, a deacetylase enzyme, is closely associated with inflammatory responses and apoptosis, playing a crucial role in the pathogenesis of various neurological disorders. This research aims to elucidate the specific mechanisms by which SIRT2 overexpression inhibits ferroptosis and promotes SCI repair through the deacetylation of nuclear factor-κB (NF-κB) p65.

Results

Utilizing cell models and a rat SCI model, we discovered that SIRT2 overexpression promotes NF-κB p65 deacetylation, subsequently inhibiting ferroptosis and oxidative stress. C

SUBMITTER: Shi S 

PROVIDER: S-EPMC12613685 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature