ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015
STAT-dependent upregulation of 12/15-lipoxygenase contributes to neuronal injury after stroke.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Lipoxygenase (LOX) signaling in epilepsy: Pathophysiology and therapeutic prospects.Neurobiology of disease · 2026Review
- Ferroptosis in neurological diseases: moving towards therapeutic intervention.Molecular psychiatry · 2026Review
- Status epilepticus-induced 12/15-lipoxygenase drives neuroinflammation and contributes to neuronal injuries and behavioral comorbidities.Acta pharmacologica Sinica · 2026Article
- STAT6-Mediated SOCS2 Alleviates Cognitive Impairments and Neuronal Damage in Alzheimer's Disease Rat Models and Aβ1-42-Stimulated HT-22 Cells.Molecular neurobiology · 2026Article
- Olfactory mucosa-mesenchymal stem cells with overexpressed Nrf2 modulate angiogenesis and exert anti-inflammation effect in an in vitro traumatic brain injury model.European journal of medical research · 2025Article
- Ferroptosis in ischemic stroke: Animal models and mechanisms.Zoological research · 2024Review
- Mechanism of Efferocytosis in Determining Ischaemic Stroke Resolution-Diving into Microglia/Macrophage Functions and Therapeutic Modality.Molecular neurobiology · 2024Review
- LncRNA MALAT1 and Ischemic Stroke: Pathogenesis and Opportunities.Molecular neurobiology · 2024Review
- 12-Hydroxyeicosatetraenoic acid is the only enzymatically produced HETE increased under brain ischemia.Prostaglandins, leukotrienes, and essential fatty acids · 2024Article
- Targeted ablation of signal transducer and activator of transduction 1 alleviates inflammation by microglia/macrophages and promotes long-term recovery after ischemic stroke.Journal of neuroinflammation · 2023Article
- Stroke and Etiopathogenesis: What Is Known?Genes · 2022Review
- Intertwined Relation between the Endoplasmic Reticulum and Mitochondria in Ischemic Stroke.Oxidative medicine and cellular longevity · 2022Review
- An Integrated Analysis of Network Pharmacology and Experimental Validation to Reveal the Mechanism of Chinese Medicine Formula Naotaifang in Treating Cerebral Ischemia-Reperfusion Injury.Drug design, development and therapy · 2021Article
- Can miRNAs Be Considered as Diagnostic and Therapeutic Molecules in Ischemic Stroke Pathogenesis?-Current Status.International journal of molecular sciences · 2020Review
- Integrated analysis of the proteome and transcriptome in a MCAO mouse model revealed the molecular landscape during stroke progression.Journal of advanced research · 2020Article
- Article
- The Mitochondria-Derived Peptide Humanin Improves Recovery from Intracerebral Hemorrhage: Implication of Mitochondria Transfer and Microglia Phenotype Change.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Review
- STAT6/Arg1 promotes microglia/macrophage efferocytosis and inflammation resolution in stroke mice.JCI insight · 2019Article
- Long non-coding RNAs and cell death following ischemic stroke.Metabolic brain disease · 2019Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Oxidative stress is a major brain injury mechanism after ischemic stroke. 12/15-lipoxygenase (12/15-LOX) is a key mediator of oxidative stress, contributing to neuronal cell death and vascular leakage. Nonetheless, the mechanism leading to its upregulation is currently unknown. We show here that Signal Transducers and Activators of Transcription (STATs), specifically STAT6 and possibly STAT1, increase transcription of 12/15-LOX in neuronal cells. Both p-STAT6 and -1 bound to specific STAT binding sites in the mouse 12/15-LOX promoter. Small interfering RNA (siRNA) knockdown showed STAT6 to be the dominant regulator, reducing 12/15-LOX promoter activation and cell death in oxidatively stressed HT22 cells. STAT6 siRNA efficiently prevented the increase of 12/15-LOX in murine primary neurons, both after induction of oxidative stress and after oxygen-glucose deprivation. Early activation of STAT6 and STAT1 in mice was consistent with a role in regulating 12/15-LOX in focal ischemia. Brains of human stroke patients showed increased p-STAT6 and p-STAT1 in the peri-infarct region, along with 12/15-LOX and markers of apoptosis. These results link STAT6 and STAT1 to the 12/15-LOX damage pathway and suggest disregulation of STAT-dependent transcription as injury mechanism in stroke. Selectively targeting STATs may thus be a novel therapeutic approach to reducing brain injury after a stroke.
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Registered trials
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