ArticleScientific reports2016
TIGAR contributes to ischemic tolerance induced by cerebral preconditioning through scavenging of reactive oxygen species and inhibition of apoptosis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- TIGAR overexpression alleviates intracerebral hemorrhage injury in mice by suppressing ATF4/NOX4/p22phox-mediated oxidative stress and inflammation.Acta pharmacologica Sinica · 2026Article
- GALNT3 Inhibits the Progression of Cerebral Ischemia-Reperfusion Injury by Stabilizing TREM2 via O-GalNAc Glycosylation.CNS neuroscience & therapeutics · 2026Article
- TIGAR promotes osteogenic differentiation and ameliorates glucocorticoid-induced osteoporosis via autophagy-Nrf2-ROS axis.Genes & diseases · 2026Article
- Proteomic Analysis of Mouse Cerebral Cortex Following Experimental Ischemic Stroke: Identifying Novel Biomarkers of Damage and Repair.Cellular and molecular neurobiology · 2025Article
- N-Acety-L-Cysteine Alleviates Isoflurane-Triggered Neuronal Cell Parthanatos by Suppressing Reactive Oxygen Species Accumulation Through the Induction of c-Jun N-Terminal Kinase Signaling Pathway Inhibition.Journal of biochemical and molecular toxicology · 2025Article
- TIGAR Suppresses ER Stress-Induced Neuronal Injury through Targeting ATF4 Signaling in Cerebral Ischemia/Reperfusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Targeting intracellular autophagic process for the treatment of post-stroke ischemia/reperfusion injury.Animal models and experimental medicine · 2025Review
- Article
- Fascaplysin Induces Apoptosis and Ferroptosis, and Enhances Anti-PD-1 Immunotherapy in Non-Small Cell Lung Cancer (NSCLC) by Promoting PD-L1 Expression.International journal of molecular sciences · 2022Article
- TIGAR alleviates oxidative stress in brain with extended ischemia via a pentose phosphate pathway-independent manner.Redox biology · 2022Article
- The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022Review
- Proteomic identification of ruminal epithelial protein expression profiles in response to starter feed supplementation in pre-weaned lambs.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2021Article
- Structure, regulation, and biological functions of TIGAR and its role in diseases.Acta pharmacologica Sinica · 2021Review
- Metabolism and immunity in breast cancer.Frontiers of medicine · 2021Review
- Specificity Protein 1: A Protein With a Two-Sided Role in Ischemic Stroke.Frontiers in cellular neuroscience · 2021Review
- Exogenous NADPH ameliorates myocardial ischemia-reperfusion injury in rats through activating AMPK/mTOR pathway.Acta pharmacologica Sinica · 2020Article
- Heme Oxygenase-1 Inhibition Sensitizes Human Prostate Cancer Cells towards Glucose Deprivation and Metformin-Mediated Cell Death.International journal of molecular sciences · 2019Article
- Potent effects of dioscin against hepatocellular carcinoma through regulating TP53-induced glycolysis and apoptosis regulator (TIGAR)-mediated apoptosis, autophagy, and DNA damage.British journal of pharmacology · 2019Article
- NADPH ameliorates MPTP-induced dopaminergic neurodegeneration through inhibiting p38MAPK activation.Acta pharmacologica Sinica · 2019Article
- TIGAR Attenuates High Glucose-Induced Neuronal ApoptosisFrontiers in molecular neuroscience · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous study showed that TIGAR (TP53-induced glycolysis and apoptosis regulator) protected ischemic brain injury via enhancing pentose phosphate pathway (PPP) flux and preserving mitochondria function. This study was aimed to study the role of TIGAR in cerebral preconditioning. The ischemic preconditioning (IPC) and isoflurane preconditioning (ISO) models were established in primary cultured cortical neurons and in mice. Both IPC and ISO increased TIGAR expression in cortical neurons. Preconditioning might upregulate TIGAR through SP1 transcription factor. Lentivirus mediated knockdown of TIGAR significantly abolished the ischemic tolerance induced by IPC and ISO. ISO also increased TIGAR in mouse cortex and hippocampus and alleviated subsequent brain ischemia-reperfusion injury, while the ischemic tolerance induced by ISO was eliminated with TIGAR knockdown in mouse brain. ISO increased the production of NADPH and glutathione (GSH), and scavenged reactive oxygen species (ROS), while TIGAR knockdown decreased GSH and NADPH production and increased the level of ROS. Supplementation of ROS scavenger NAC and PPP product NADPH effectively rescue the neuronal injury caused by TIGAR deficiency. Notably, TIGAR knockdown inhibited ISO-induced anti-apoptotic effects in cortical neurons. These results suggest that TIGAR participates in the cerebral preconditioning through reduction of ROS and subsequent cell apoptosis.
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Registered trials
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