{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTP53‐induced glycolysis and apoptosis regulator (TIGAR) was first identified as a p53‐responsive gene that functions as a fructose‐2,6‐bisphosphatase. By lowering intracellular levels of fructose‐2,6‐bisphosphate, TIGAR limits glycolysis and shifts glucose metabolism toward the pentose phosphate pathway, thereby increasing NADPH production and reducing reactive oxygen species (ROS). This metabolic reprogramming not only mitigates oxidative stress but also protects cells against apoptosis and genomic damage, helping to maintain cellular homeostasis under mild or transient stress conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nUnder conditions of nutrient deprivation, hypoxia, or exposure to chemotherapeutics, TIGAR activity is further modulated via various post‐translational and transcriptional mechanisms. Its ability to localize to mitochondria and interact with key metabolic enzymes (for example, hexokinase 2) under stress facilitates additional control over mitochondrial ROS. Moreover, TIGAR’s regulation via alternative pathways—including acetylation and microRNA‐mediated mechanisms—enables it to play dual roles in tumor biology: on one hand protecting cancer cells by lowering ROS and inhibiting apoptosis and autophagy, and on the other hand contributing to metabolic compartmentalization that supports tumor growth, metastasis, and even ferroptosis resistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical regulation by p53, TIGAR expression is controlled by multiple additional factors, including CREB, NRF2, TCF19, and specific microRNAs. These alternative regulatory inputs allow TIGAR to integrate oncogenic, metabolic, and stress signals in a cell type‐ and context‐dependent manner. Dysregulation of TIGAR has been observed in a broad range of pathological contexts, including various cancers (such as breast, colorectal, glioma, pancreatic, gastric, and nasopharyngeal carcinomas), neurodegeneration, ischemia, and even kidney injury through modulation of ferroptosis. Its impact on treatment responsiveness is notable, as altered TIGAR levels can influence radiosensitivity, chemoresistance, and cell death pathways. Together, these findings position TIGAR not only as a central mediator of metabolic reprogramming and redox control but also as a promising therapeutic target for both cancer and non‐cancer diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Karim Bensaad, Atsushi Tsuruta, Mary A Selak, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "TIGAR is required for efficient intestinal regeneration and tumorigenesis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Dev Cell (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.devcel.2013.05.001"}], "href": "https://doi.org/10.1016/j.devcel.2013.05.001"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23726973"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23726973"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Shubiao Zou, Xiaozhong Wang, Linqiang Deng, et al. 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