ReviewFrontiers in immunology2022
Perspectives on the mechanism of pyroptosis after intracerebral hemorrhage.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Mechanisms of exercise-based rehabilitation following intracerebral hemorrhage: insights from preclinical evidence.Frontiers in pharmacology · 2026Pooled it
- Thymosin β4 Mitigates Acute Cerebral Infarction Via Inhibition of the TLR4/NF-κB Pathway and Suppression of Neuronal Pyroptosis.Applied biochemistry and biotechnology · 2026Article
- Gasdermin D in Neurodegenerative Diseases: Pathogenic Roles and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- Development of a Novel Prognostic Inflammation Index to Predict Poor Outcomes in Patients With Intracerebral Hemorrhage: A Longitudinal Study.CNS neuroscience & therapeutics · 2026Article
- Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting.Neuromolecular medicine · 2026Review
- Healthy young human plasma-derived exosomes enhance neural stem cell therapy by suppressing pyroptosis via TXNIP/NLRP3 after intracerebral hemorrhage.Journal of nanobiotechnology · 2026Article
- Rhein Inhibits NLRP3 Activation and Alleviates Microglial Pyroptosis After Intracerebral Hemorrhage in Rats.Brain and behavior · 2026Article
- Neuroprotective effect of sinomenine on parkinson's disease through NLRP3/Caspase-1/GSDMD pathway-mediated pyroptosis inhibition.Metabolic brain disease · 2026Article
- Advances in the mechanisms of electroacupuncture in the treatment of cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2026Review
- Inhibition of the Sp1/CTR1 axis attenuates cuproptosis and alleviates axonal injury following intracerebral hemorrhage.Frontiers in molecular biosciences · 2026Article
- Single-nucleus transcriptomic profiling reveals temporal dynamics of neuroinflammation and myelin repair after intracerebral haemorrhage.Clinical and translational medicine · 2025Article
- Exosomal MicroRNA: an Effective Strategy for the Treatment of Intracerebral Hemorrhage.Molecular neurobiology · 2025Review
- CPT1A mediated preservation of mitochondrial inhibits pyroptosis in pancreatic acinar cells.Frontiers in cell and developmental biology · 2025Article
- Targeting glial cell pyroptosis and neuroinflammation in post-stroke depression: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2025Review
- Disulfiram attenuates cell and tissue damage and blood‒brain barrier dysfunction after intracranial haemorrhage by inhibiting the classical pyroptosis pathway.Scientific reports · 2024Article
- Treatment of Intracerebral Hemorrhage with Traditional Chinese Medicine Monomer Wogonin by Modifying NLRP3 with METTL14 to Inhibit Neuronal Cell Pyroptosis.Applied biochemistry and biotechnology · 2024Article
- P2Y6 Receptor Activation Aggravates NLRP3-dependent Microglial Pyroptosis via Downregulation of the PI3K/AKT Pathway in a Mouse Model of Intracerebral Hemorrhage.Molecular neurobiology · 2024Article
- Peroxiredoxin II exerts neuroprotective effects by inhibiting endoplasmic reticulum stress and oxidative stress-induced neuronal pyroptosis.Molecular biology reports · 2024Article
- The Mechanism of Astragaloside IV in NOD-like Receptor Family Pyrin Domain Containing 3 Inflammasome-mediated Pyroptosis after Intracerebral Hemorrhage.Current neurovascular research · 2024Article
- Knockdown of LCN2 Attenuates Brain Injury After Intracerebral Hemorrhage via Suppressing Pyroptosis.Neuropsychiatric disease and treatment · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) is a highly harmful neurological disorder with high rates of mortality, disability, and recurrence. However, effective therapies are not currently available. Secondary immune injury and cell death are the leading causes of brain injury and a poor prognosis. Pyroptosis is a recently discovered form of programmed cell death that differs from apoptosis and necrosis and is mediated by gasdermin proteins. Pyroptosis is caused by multiple pathways that eventually form pores in the cell membrane, facilitating the release of inflammatory substances and causing the cell to rupture and die. Pyroptosis occurs in neurons, glial cells, and endothelial cells after ICH. Furthermore, pyroptosis causes cell death and releases inflammatory factors such as interleukin (IL)-1β and IL-18, leading to a secondary immune-inflammatory response and further brain damage. The NOD-like receptor protein 3 (NLRP3)/caspase-1/gasdermin D (GSDMD) pathway plays the most critical role in pyroptosis after ICH. Pyroptosis can be inhibited by directly targeting NLRP3 or its upstream molecules, or directly interfering with caspase-1 expression and GSDMD formation, thus significantly improving the prognosis of ICH. The present review discusses key pathological pathways and regulatory mechanisms of pyroptosis after ICH and suggests possible intervention strategies to mitigate pyroptosis and brain dysfunction after ICH.
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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.