Autophagy activation by the Becn1^F121A mutation reprograms neuroinflammation and promotes neurological recovery after spinal cord injury.

ABSTRACT: Autophagy is essential for maintaining cellular homeostasis, particularly under stress conditions such as neurotrauma. In experimental models of spinal cord injury (SCI), dysregulated autophagy has been closely associated with secondary injury cascades. Our previous work demonstrated that post-injury inflammation is exacerbated by genetic inhibition of autophagy and alleviated by pharmacological enhancement. Emerging evidence also indicates that SCI can induce neuropathological changes in the brain, leading to cognitive impairments; however, the underlying molecular mechanisms remain largely unclear. In this study, we utilized Becn1^F121A/F121A knock-in (BMut) mice to investigate how genetically enhanced autophagy influences transcriptomic profiles, neural cell responses, tissue

SUBMITTER: Lei Z 

PROVIDER: S-EPMC12821155 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature