ArticleScientific reports2019
Targeting PFKFB3 alleviates cerebral ischemia-reperfusion injury in mice.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Maternal Inflammation Alters Nuclear and Mitochondrial DNA Methylation Patterns in Neonatal Brain Monocytes.Cells · 2026Article
- F26BP enables control of glycolysis rate independent of energy state.bioRxiv : the preprint server for biology · 2026Article
- Glucose Metabolic Enzyme PFKFB3 in Cardiopulmonary Vascular Health and Disease.Circulation research · 2026Review
- Endogenous mitochondrial hydrogen peroxide regulates neurogenesis during cortical development.Redox biology · 2025Article
- Glycolytic Enzyme HK2 Phosphorylates nSMase1 to Promote Astrocytic Exosomes Biogenesis Contributing to Acute Ischemic Stroke Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Temporal characterisation and electrophysiological implications of TBI-induced serine/threonine kinase activity in mouse cortex.Cellular and molecular life sciences : CMLS · 2025Article
- The small molecule inhibitor 3PO is a modulator of neutrophil metabolism, ROS production, and NET release.Clinical and experimental immunology · 2025Article
- The impact of glycolysis on ischemic stroke: from molecular mechanisms to clinical applications.Frontiers in neurology · 2025Review
- Metabolism in the tumor microenvironment: implications for pathogenesis and therapeutics.Frontiers in immunology · 2025Review
- Exploring the molecular mechanisms of Pueraria in Alzheimer's disease treatment using machine learning and network pharmacology.Frontiers in nutrition · 2025Article
- Targeting glycolysis for neuroprotection in early LPS-induced neuroinflammation.Brain, behavior, & immunity - health · 2024Article
- PFKFB3 ameliorates ischemia-induced neuronal damage by reducing reactive oxygen species and inhibiting nuclear translocation of Cdk5.Scientific reports · 2024Article
- The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024Review
- Intracellular BAPTA directly inhibits PFKFB3, thereby impeding mTORC1-driven Mcl-1 translation and killing MCL-1-addicted cancer cells.Cell death & disease · 2023Article
- Neurons require glucose uptake and glycolysis in vivo.Cell reports · 2023Article
- The Duration of Oxygen and Glucose Deprivation (OGD) Determines the Effects of Subsequent Reperfusion on Rat Pheochromocytoma (PC12) Cells and Primary Cortical Neurons.International journal of molecular sciences · 2023Article
- Cross-talk between energy and redox metabolism in astrocyte-neuron functional cooperation.Essays in biochemistry · 2023Review
- Leptin accelerates BMSC transformation into vertebral epiphyseal plate chondrocytes by activating SENP1-mediated deSUMOylation of SIRT3.FEBS open bio · 2023Article
- Senescent melanocytes driven by glycolytic changes are characterized by melanosome transport dysfunction.Theranostics · 2023Article
- Advances in Human Mitochondria-Based Therapies.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glycolytic rate in neurons is low in order to allow glucose to be metabolized through the pentose-phosphate pathway (PPP), which regenerates NADPH to preserve the glutathione redox status and survival. This is controlled by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3), the pro-glycolytic enzyme that forms fructose-2,6-bisphosphate, a powerful allosteric activator of 6-phosphofructo-1-kinase. In neurons, PFKFB3 protein is physiologically inactive due to its proteasomal degradation. However, upon an excitotoxic stimuli, PFKFB3 becomes stabilized to activate glycolysis, thus hampering PPP mediated protection of redox status leading to neurodegeneration. Here, we show that selective inhibition of PFKFB3 activity by the small molecule AZ67 prevents the NADPH oxidation, redox stress and apoptotic cell death caused by the activation of glycolysis triggered upon excitotoxic and oxygen-glucose deprivation/reoxygenation models in mouse primary neurons. Furthermore, in vivo administration of AZ67 to mice significantly alleviated the motor discoordination and brain infarct injury in the middle carotid artery occlusion ischemia/reperfusion model. These results show that pharmacological inhibition of PFKFB3 is a suitable neuroprotective therapeutic strategy in excitotoxic-related disorders such as stroke.
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