ArticleCell transplantation
6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase Suppresses Neuronal Apoptosis by Increasing Glycolysis and "cyclin-dependent kinase 1-Mediated Phosphorylation of p27 After Traumatic Spinal Cord Injury in Rats.
Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Adipose tissue-derived stromal cells enhance glycolytic metabolism in injured nerve cells via the FOXK1-HK2 axis for spinal cord injury repair.Journal of translational medicine · 2026Article
- Metabolic Reprogramming in Spinal Cord Injury and Analysis of Potential Therapeutic Targets.Journal of molecular neuroscience : MN · 2025Article
- MCT1-mediated endothelial cell lactate shuttle as a target for promoting axon regeneration after spinal cord injury.Theranostics · 2024Article
- The role of kinases in peripheral nerve regeneration: mechanisms and implications.Frontiers in neurology · 2024Review
- Pathogenic role of PFKFB3 in endothelial inflammatory diseases.Frontiers in molecular biosciences · 2024Review
- PFKFB3 downregulation aggravates Angiotensin II-induced podocyte detachment.Renal failure · 2023Article
- Molecular Aspects of Hypoxic Stress Effects in Chronic Ethanol Exposure of Neuronal Cells.Current issues in molecular biology · 2023Article
- The Impact of Sex Chromosomes in the Sexual Dimorphism of Pulmonary Arterial Hypertension.The American journal of pathology · 2022Review
- Stat3-Induced lncRNA Kcnq1ot1 Regulates the Apoptosis of Neuronal Cells in Spinal Cord Injury.Journal of molecular neuroscience : MN · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis is a vital pathological factor that accounts for the poor prognosis of traumatic spinal cord injury (t-SCI). The 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) is a critical regulator for energy metabolism and proven to have antiapoptotic effects. This study aimed to investigate the neuroprotective role of PFKFB3 in t-SCI. A compressive clip was introduced to establish the t-SCI model. Herein, we identified that PFKFB3 was extensively distributed in neurons, and PFKFB3 levels significantly increased and peaked 24 h after t-SCI. Additionally, knockdown of PFKFB3 inhibited glycolysis, accompanied by aggravated neuronal apoptosis and white matter injury, while pharmacological activation of PFKFB3 with meclizine significantly enhanced glycolysis, attenuated t-SCI-induced spinal cord injury, and alleviated neurological impairment. The PFKFB3 agonist, meclizine, activated cyclin-dependent kinase 1 (CDK1) and promoted the phosphorylation of p27, ultimately suppressing neuronal apoptosis. However, the neuroprotective effects of meclizine against t-SCI were abolished by the CDK1 antagonist, RO3306. In summary, our data demonstrated that PFKFB3 contributes robust neuroprotection against t-SCI by enhancing glycolysis and modulating CDK1-related antiapoptotic signals. Moreover, targeting PFKFB3 may be a novel and promising therapeutic strategy for t-SCI.
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