ReviewEpilepsia open2023
Programmed mechanisms of status epilepticus-induced neuronal necrosis.
Review in Epilepsia open, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Differential Effects of Hypoglycemia and Excitotoxic Signals on SN56 Septal Cholinergic Neuronal Cells.Cells · 2026Article
- Ginsenoside Rh2 Protects Against Glutamate-Induced Neurotoxicity in PC12 Cells via Activation of the VEGF-mediated PI3K/Akt/mTOR Signaling Pathway.Neurochemical research · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Bcl-2 and FAS as Apoptosis-Related Markers in Patients with Convulsive Status Epilepticus.Journal of clinical medicine · 2025Article
- Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025Review
- Review
- Association between the postoperative glycemic variability and mortality after craniotomy: a retrospective cohort study and development of a mortality prediction model.Frontiers in endocrinology · 2025Article
- Acupuncture for Ischemic Stroke: A Critical Evaluation of Biological Mechanisms and Methodological Challenges.International journal of general medicine · 2025Review
- Emergent responsive neurostimulation in pediatric super-refractory epilepsia partialis continua.Annals of clinical and translational neurology · 2024Article
- ER and doctors' preparedness to manage status epilepticus: a multi-institutional survey from the Gaza Strip.BMC health services research · 2024Article
- Mechanisms of Organophosphate Toxicity and the Role of Acetylcholinesterase Inhibition.Toxics · 2023Review
- Programmed mechanisms of status epilepticus-induced neuronal necrosis.Epilepsia open · 2023Review
- Reactive oxygen species in status epilepticus.Epilepsia open · 2023Article
- EGCG Attenuates CA1 Neuronal Death by Regulating GPx1, NF-κB S536 Phosphorylation and Mitochondrial Dynamics in the Rat Hippocampus following Status Epilepticus.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Excitotoxicity is the underlying mechanism for all acute neuronal injury, from cerebral ischemia, status epilepticus, traumatic CNS injury, and hypoglycemia. It causes morphological neuronal necrosis, and it triggers a programmed cell death program. Excessive calcium entry through the NMDA-receptor-operated cation channel activates two key enzymes-calpain I and neuronal nitric oxide synthase (nNOS). Calpain I, a cytosolic enzyme, translocates to mitochondrial and lysosomal membranes, causing release of cytochrome c, endonuclease G, and apoptosis-inducing factor (AIF) from mitochondria and DNase II and cathepsins B and D from lysosomes. These all translocate to neuronal nuclei, creating DNA damage, which activates poly(ADP) ribose polymerase-1 (PARP-1) to form excessive amounts of poly(ADP) ribose (PAR) polymers, which translocate to mitochondrial membranes, causing release of truncated AIF (tAIF). The free radicals that are released from mitochondria and peroxynitrite, formed from nitric oxide (NO) from nNOS catalysis of L-arginine to L-citrulline, damage mitochondrial and lysosomal membranes and DNA. The end result is the necrotic death of neurons. Another programmed necrotic pathway, necroptosis, occurs through a parallel pathway. As investigators of necroptosis do not recognize the excitotoxic pathway, it is unclear to what extent each contributes to programmed neuronal necrosis. We are studying the extent to which each contributes to acute neuronal necrosis and the extent of cross-talk between these pathways.
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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.