ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2013
Transglutaminase is a therapeutic target for oxidative stress, excitotoxicity and stroke: a new epigenetic kid on the CNS block.
Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Partial TG6 loss of function causes motor deficits in male mice.Human molecular genetics · 2026Article
- The cross-linking activity of transglutaminase 2 drives α-Synuclein pathology in synucleinopathy models.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Oxidative markers and SOD variant: predictors of autism severity and susceptibility.Future science OA · 2025Article
- Factors influencing brain recovery from stroke via possible epigenetic changes.Future science OA · 2024Review
- Article
- Pharmacological inhibition of astrocytic transglutaminase 2 facilitates the expression of a neurosupportive astrocyte reactive phenotype in association with increased histone acetylation.bioRxiv : the preprint server for biology · 2024Article
- Biological Implications and Functional Significance of Transglutaminase Type 2 in Nervous System Tumors.Cells · 2024Review
- Ion Channel Dysregulation Following Intracerebral Hemorrhage.Neuroscience bulletin · 2024Review
- Pathogenetic Contributions and Therapeutic Implications of Transglutaminase 2 in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Article
- XJB-5-131 Is a Mild Uncoupler of Oxidative Phosphorylation.Journal of Huntington's disease · 2022Article
- Neither a Novel Tau Proteinopathy nor an Expansion of a Phenotype: Reappraising Clinicopathology-Based Nosology.International journal of molecular sciences · 2021Article
- Epigenetic regulators of neuronal ferroptosis identify novel therapeutics for neurological diseases: HDACs, transglutaminases, and HIF prolyl hydroxylases.Neurobiology of disease · 2021Review
- Amino acid metabolism, lipid metabolism, and oxidative stress are associated with post-stroke depression: a metabonomics study.BMC neurology · 2020Article
- The Chemical Biology of Ferroptosis in the Central Nervous System.Cell chemical biology · 2020Review
- Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to repair the genome and improve stroke recovery.Neuropharmacology · 2018Review
- P2X7 Receptor-Associated Programmed Cell Death in the Pathophysiology of Hemorrhagic Stroke.Current neuropharmacology · 2018Review
- Striatal Mutant Huntingtin Protein Levels Decline with Age in Homozygous Huntington's Disease Knock-In Mouse Models.Journal of Huntington's disease · 2018Article
- The gliadin peptide 31-43 exacerbates kainate neurotoxicity in epilepsy models.Scientific reports · 2017Article
- Noise-Induced Hepatic Stress Is Associated with Transglutaminase Activation and TG7 Upregulation in Rats.Noise & healthArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Transglutaminases (TGs) are multifunctional, calcium-dependent enzymes that have been recently implicated in stroke pathophysiology. Classically, these enzymes are thought to participate in cell injury and death in chronic neurodegenerative conditions via their ability to catalyze covalent, nondegradable crosslinks between proteins or to incorporate polyamines into protein substrates. Accumulating lines of inquiry indicate that specific TG isoforms can shuttle into the nucleus when they sense pathologic changes in calcium or oxidative stress, bind to chromatin and thereby transduce these changes into transcriptional repression of genes involved in metabolic or oxidant adaptation. Here, we review the evidence that supports principally a role for one isoform of this family, TG2, in cell injury and death associated with hemorrhagic or ischemic stroke. We also outline an evolving model in which TG2 is a critical mediator between pathologic signaling and epigenetic modifications that lead to gene repression. Accordingly, the salutary effects of TG inhibitors in stroke may derive from their ability to restore homeostasis by removing inappropriate deactivation of adaptive genetic programs by oxidative stress or extrasynaptic glutamate receptor signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.