SVF
Level D· Preclinical EvidenceAnimal Study

Adipose tissue-derived stromal cells enhance glycolytic metabolism in injured nerve cells via the FOXK1-HK2 axis for spinal cord injury repair.

Li F., Li H., Jia Y., Ou L., Fang Y., Pan L.

Animal Study on Spinal Cord Injury, published in J Transl Med (2026) — summary generated from the PubMed abstract.

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
J Transl Med (2026)
Country
England
Reported sample size
—
PMID
41845409
DOI
10.1186/s12967-026-07958-w

Abstract (original English)

BACKGROUND: Spinal cord injury (SCI) causes severe energy metabolism dysfunction, hindering neuronal survival and recovery. Adipose tissue-derived stromal cells (ADSCs) have neuroprotective potential, but their role in regulating neuronal energy metabolism and the underlying mechanisms remain unclear. This study aimed to investigate whether ADSCs are capable of restoring neuronal glycolysis through the FOXK1-HK2 signaling pathway, thereby replenishing the energy supply and facilitating tissue regeneration. METHODS: We employed rat and cell models of SCI to observe the effects of ADSCs on glycolytic metabolism and apoptosis. Transcriptome sequencing identified glycolysis-related differentially expressed genes. Lactate detection and Seahorse assays were used to quantify glycolytic activity. Dual-luciferase reporter assays verified the FOXK1-HK2 regulatory relationship. Cut&Run assay provided direct evidence of FOXK1 binding to the HK2 promoter. Behavioral tests, histopathological staining and immunofluorescence were used to evaluate in vivo functional recovery and tissue repair. FOXK1 knockdown confirmed its role in the ADSC-mediated pathway. RESULTS: We found that ADSCs exerted multiple protective and regulatory effects on neurons and motor function. Specifically, they strongly inhibited neuronal oxidative stress, protected mitochondria, and promoted neuronal metabolic reprogram

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence comes from animal or laboratory studies and has not been confirmed in humans.

How we grade evidence
AnimalsGlycolysisForkhead Transcription FactorsSpinal Cord InjuriesStromal CellsNeuronsAdipose TissueSignal TransductionHexokinaseRats, Sprague-Dawley
Back & SpineHipSpinal Cord Injury
View on PubMedDOI

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