ArticleScientific reports2017
Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 115 citations in OpenAlex.
- Neuroimmune-oligovascular signaling shapes oligodendrocyte precursor cell fate and repair after ischemic stroke.Cell communication and signaling : CCS · 2026Review
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Article
- RIPK3 Protects Against Endothelial Activation and Vascular Permeability in a Mouse Model of Ischemia-Reperfusion Injury.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Resveratrol reduces muscle atrophy and stress pathway activation in a combined disuse-hypoxia-mouse model.Frontiers in pharmacology · 2026Article
- Crosstalk between autophagy-dependent ferroptosis and PANoptosis in myocardial and cerebral ischemia-reperfusion injury: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- HIF-1α at the intersection of hypoxia, ferroptosis-associated stress, and cell death crosstalk in osteomyelitis.Frontiers in cell and developmental biology · 2026Review
- The molecular mechanisms and therapeutic implications of PANoptosis in ischemic diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- RIPK1: A Promising Target for Intervention Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Necrosis-like cell death modes in heart failure: the influence of aetiology and the effects of RIP3 inhibition.Basic research in cardiology · 2025Article
- Neuregulin-1 prevents death from a normally lethal respiratory viral infection.PLoS pathogens · 2025Article
- Hypoxia-mediated SUMOylation of FADD exacerbates endothelial cell injury via the RIPK1-RIPK3-MLKL signaling axis.Cell death & disease · 2025Article
- Deciphering Necroptosis-Associated Molecular Subtypes in Acute Ischemic Stroke Through Bioinformatics and Machine Learning Analysis.Journal of molecular neuroscience : MN · 2025Article
- The Therapeutic Effects of Blueberry-Treated Stem Cell-Derived Extracellular Vesicles in Ischemic Stroke.International journal of molecular sciences · 2024Article
- The protective role of endothelial GLUT1 in ischemic stroke.Brain and behavior · 2024Review
- Article
- Insight into interplay between PANoptosis and autophagy: novel therapeutics in ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- HIF-1α promotes astrocytic production of macrophage migration inhibitory factor following spinal cord injury.CNS neuroscience & therapeutics · 2023Article
- Sugarcane leaf polysaccharide exerts a therapeutic effect on cardiovascular diseases through necroptosis.Heliyon · 2023Article
- Necroptosis inhibition counteracts neurodegeneration, memory decline, and key hallmarks of aging, promoting brain rejuvenation.Aging cell · 2023Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis, a novel type of programmed cell death, is involved in stroke-induced ischemic brain injury. Although studies have sought to explore the mechanisms of necroptosis, its signaling pathway has not yet to be completely elucidated. Thus, we used oxygen-glucose deprivation (OGD) and middle cerebral artery occlusion (MCAO) models mimicking ischemic stroke (IS) conditions to investigate mechanisms of necroptosis. We found that OGD and MCAO induced cell death, local brain ischemia and neurological deficit, while zVAD-fmk (zVAD, an apoptotic inhibitor), GSK'872 (a receptor interacting protein kinase-3 (RIP3) inhibitor), and combined treatment alleviated cell death and ischemic brain injury. Moreover, OGD and MCAO upregulated protein expression of the triggers of necroptosis: receptor interacting protein kinase-1 (RIP1), RIP3 and mixed lineage kinase domain-like protein (MLKL). The upregulation of these proteins was inhibited by GSK'872, combination treatments and RIP3 siRNA but not zVAD treatment. Intriguingly, hypoxia-inducible factor-1 alpha (HIF-1α), an important transcriptional factor under hypoxic conditions, was upregulated by OGD and MCAO. Similar to their inhibitory effects on aforementioned proteins upregulation, GSK'872, combination treatments and RIP3 siRNA decreased HIF-1α protein level. These findings indicate that necroptosis contributes to ischemic brain injury induced by OGD and MCAO and implicate HIF-1α, RIP1, RIP3, and MLKL in necroptosis.
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