ArticleFrontiers in molecular neuroscience2019
TIGAR Attenuates High Glucose-Induced Neuronal Apoptosis
Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Physiological levels of 3-hydroxykynurenine alter mitochondrial function and morphology in neuronal cells.bioRxiv : the preprint server for biology · 2026Article
- Targeting p75NTR activity alleviates the neurotoxic effect of high glucose on iPSC-derived dopaminergic neurons.Stem cell research & therapy · 2026Article
- TIGAR regulates intestinal mucus barrier integrity by inhibiting lactylation of G6PD/6PGD in ulcerative colitis.Nature communications · 2026Article
- Exercise Training Alters the Hippocampal Expression of Blood-Brain Barrier Components and Behavior of Western Diet-Fed Female Rats.Molecular neurobiology · 2025Article
- Nitric oxide synthase 1 inhibits the progression of esophageal cancer through interacting with nitric oxide synthase 1 adaptor protein.World journal of gastrointestinal oncology · 2025Article
- Diabetes exerts a causal impact on the nervous system within the right hippocampus: substantiated by genetic data.Endocrine · 2025Article
- Mechanistic Insights and Potential Therapeutic Implications of NRF2 in Diabetic Encephalopathy.Molecular neurobiology · 2024Review
- HDAC1 Promotes Mitochondrial Pathway Apoptosis and Inhibits the Endoplasmic Reticulum Stress Response in High Glucose-Treated Schwann Cells via Decreased U4 Spliceosomal RNA.Neurochemical research · 2024Article
- Different Types of Cell Death in Diabetic Neuropathy: A Focus on Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- The Multiple Roles of Autophagy in Neural Function and Diseases.Neuroscience bulletin · 2024Review
- Characterizing the metabolic divide: distinctive metabolites differentiating CAD-T2DM from CAD patients.Cardiovascular diabetology · 2024Article
- Pyruvate dehydrogenase kinase 1 protects against neuronal injury and memory loss in mouse models of diabetes.Cell death & disease · 2023Article
- Cognitive dysfunction in diabetes: abnormal glucose metabolic regulation in the brain.Frontiers in endocrinology · 2023Review
- Downregulation ofIranian journal of pharmaceutical research : IJPR · 2022Article
- Comparable Benefits of Stingless Bee Honey and Caffeic Acid in Mitigating the Negative Effects of Metabolic Syndrome on the Brain.Antioxidants (Basel, Switzerland) · 2022Article
- TIGAR alleviates oxidative stress in brain with extended ischemia via a pentose phosphate pathway-independent manner.Redox biology · 2022Article
- mTOR-mediated autophagy in the hippocampus is involved in perioperative neurocognitive disorders in diabetic rats.CNS neuroscience & therapeutics · 2022Article
- Autophagy and Diabetic Encephalopathy: Mechanistic Insights and Potential Therapeutic Implications.Aging and disease · 2022Review
- MiR-652-5p elevated glycolysis level by targeting TIGAR in T-cell acute lymphoblastic leukemia.Cell death & disease · 2022Article
- Research progress on the relationship between autophagy and chronic complications of diabetes.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia-induced neuronal apoptosis is one of the important reasons for diabetic neuropathy. Long-time exposure to high glucose accelerates many aberrant glucose metabolic pathways and eventually leads to neuronal injury. However, the underlying mechanisms of metabolic alterations remain unknown. TP53-inducible glycolysis and apoptosis regulator (TIGAR) is an endogenous inhibitor of glycolysis and increases the flux of pentose phosphate pathway (PPP) by regulating glucose 6-phosphate dehydrogenase (G6PD). TIGAR is highly expressed in neurons, but its role in hyperglycemia-induced neuronal injury is still unclear. In this study, we observed that TIGAR and G6PD are decreased in the hippocampus of streptozotocin (STZ)-induced diabetic mice. Correspondingly, in cultured primary neurons and Neuro-2a cell line, stimulation with high glucose induced significant neuronal apoptosis and down-regulation of TIGAR expression. Overexpression of TIGAR reduced the number of TUNEL-positive neurons and prevented the activation of Caspase-3 in cultured neurons. Furthermore, enhancing the expression of TIGAR rescued high glucose-induced autophagy impairment and the decrease of G6PD. Nitric oxide synthase 1 (NOS1), a negative regulator of autophagy, is also inhibited by overexpression of TIGAR. Inhibition of autophagy abolished the protective effect of TIGAR in neuronal apoptosis in Neuro-2a. Importantly, overexpression of TIGAR in the hippocampus ameliorated STZ-induced cognitive impairment in mice. Therefore, our data demonstrated that TIGAR may have an anti-apoptosis effect
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