Impairment of autophagy after spinal cord injury potentiates neuroinflammation and motor function deficit in mice.

ABSTRACT: Autophagy is a catabolic process that degrades cytoplasmic constituents and organelles in the lysosome, thus serving an important role in cellular homeostasis and protection against insults. We previously reported that defects in autophagy contribute to neuronal cell damage in traumatic spinal cord injury (SCI). Recent data from other inflammatory models implicate autophagy in regulation of immune and inflammatory responses, with low levels of autophagic flux associated with pro-inflammatory phenotypes. In the present study, we examined the effects of genetically or pharmacologically manipulating autophagy on posttraumatic neuroinflammation and motor function after SCI in mice. Methods: Young adult male C57BL/6, CX3CR1-GFP, autophagy hypomorph Becn1^+/- mice, and th

SUBMITTER: Li Y 

PROVIDER: S-EPMC9330534 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature