ArticleOxidative medicine and cellular longevity2023
Hemoglobin Derived from Subarachnoid Hemorrhage-Induced Pyroptosis of Neural Stem Cells via ROS/NLRP3/GSDMD Pathway.
Article in Oxidative medicine and cellular longevity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanisms and biomarkers of poststroke cognitive impairment.Neural regeneration research · 2026Article
- Rosiglitazone alleviates white matter injury by inhibiting NLRP3/capspase-1 mediated microglial pyroptosis via downregulating KLF4.Experimental brain research · 2026Article
- Healthy young human plasma-derived exosomes enhance neural stem cell therapy by suppressing pyroptosis via TXNIP/NLRP3 after intracerebral hemorrhage.Journal of nanobiotechnology · 2026Article
- Synergistic Combination of Hypericin-Mediated Photodynamic Therapy and HIF-1α siRNA Inhibits Triple-Negative Breast Cancer via Inducing PANoptosis in vitro.Cancer management and research · 2026Article
- Mechanisms and interventions in aneurysmal subarachnoid hemorrhage: Unraveling the role of inflammatory responses and cell death in early brain injury (Review).Molecular medicine reports · 2025Review
- Cerebrospinal fluid analysis and changes over time in patients with subarachnoid hemorrhage: a prospective observational study.Journal of anesthesia, analgesia and critical care · 2025Article
- Neuroinflammation Targeting Pyroptosis: Molecular Mechanisms and Therapeutic Perspectives in Stroke.Molecular neurobiology · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence has demonstrated that neural stem cells (NSCs) have regenerative capacity after brain injuries, such as in aneurysmal subarachnoid hemorrhage (SAH). The reactive oxygen species (ROS)-induced NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome triggers inflammatory responses and pyroptosis of cells; however, whether ROS-induced neuroinflammation modulates the fate of endogenous NSCs after SAH remains largely unknown. In this study, the level of IL-1
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Registered trials
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