MCT1-mediated endothelial cell lactate shuttle as a target for promoting axon regeneration after spinal cord injury.
Ontology highlight
ABSTRACT: Rationale: Spinal cord injury (SCI)-induced vascular damage causes ischemia and hypoxia at the injury site, which, in turn, leads to profound metabolic disruptions. The effects of these metabolic alterations on neural tissue remodeling and functional recovery have yet to be elucidated. The current study aimed to investigate the consequences of the SCI-induced hypoxic environment at the epicenter of the injury. Methods: This study employed metabolomics to assess changes in energy metabolism after SCI. The use of a lactate sensor identified lactate shuttle between endothelial cells (ECs) and neurons. Reanalysis of single-cell RNA sequencing data demonstrated reduced MCT1 expression in ECs after SCI. Additionally, an adeno-associated virus (AAV) overexpressing MCT1 was utilized
SUBMITTER: Shi C
PROVIDER: S-EPMC11413787 | biostudies-literature | 2024
REPOSITORIES: biostudies-literature
ACCESS DATA