ArticleFrontiers in cellular neuroscience2013
Contribution of apoptosis-associated signaling pathways to epileptogenesis: lessons from Bcl-2 family knockouts.
Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 73 citations in OpenAlex.
- Single-nucleus transcriptomic analysis reveals subfield-specific cell-to-cell synaptic reorganisation of the mouse hippocampus in focal temporal lobe epilepsy.Journal of translational medicine · 2026Article
- Apoptosis and Glial Marker Profiles in Hippocampus and Amygdala of Medically Intractable Temporal Lobe Epilepsy.Journal of cellular and molecular medicine · 2026Article
- Identifying the shared genes and their related microRNAs, metabolites, and pathways in ischemic stroke and epilepsy.Scientific reports · 2026Article
- Bcl-2 and FAS as Apoptosis-Related Markers in Patients with Convulsive Status Epilepticus.Journal of clinical medicine · 2025Article
- Impact of LITAF on Mitophagy and Neuronal Damage in Epilepsy via MCL-1 Ubiquitination.CNS neuroscience & therapeutics · 2025Article
- LPM682000012, a Synthetic Neuroactive Steroid That Ameliorates Epileptic Seizures by Downregulating theMolecules (Basel, Switzerland) · 2024Article
- Metabolic Adaptation in Epilepsy: From Acute Response to Chronic Impairment.International journal of molecular sciences · 2024Article
- Mechanistic insight of curcumin: a potential pharmacological candidate for epilepsy.Frontiers in pharmacology · 2024Review
- Alpha-Pinene Exerts Antiseizure Effects by Preventing Oxidative Stress and Apoptosis in the Hippocampus in a Rat Model of Temporal Lobe Epilepsy Induced by Kainate.Molecular neurobiology · 2023Article
- Dopamine, Immunity, and Disease.Pharmacological reviews · 2023Review
- Relationship between Neuroglial Apoptosis and Neuroinflammation in the Epileptic Focus of the Brain and in the Blood of Patients with Drug-Resistant Epilepsy.International journal of molecular sciences · 2022Article
- The role of peptidyl-prolyl isomerase Pin1 in neuronal signaling in epilepsy.Frontiers in molecular neuroscience · 2022Review
- Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021Review
- Inhibition of microRNA-129-2-3p protects against refractory temporal lobe epilepsy by regulating GABRA1.Brain and behavior · 2021Article
- Two Faces of Autophagy in the Struggle against Cancer.International journal of molecular sciences · 2021Review
- Notch Signaling Regulates Microglial Activation and Inflammatory Reactions in a Rat Model of Temporal Lobe Epilepsy.Neurochemical research · 2018Article
- Follow-Up of Peripheral IL-1β and IL-6 and Relation with Apoptotic Death in Drug-Resistant Temporal Lobe Epilepsy Patients Submitted to Surgery.Behavioral sciences (Basel, Switzerland) · 2018Article
- Metabolic Dysfunction and Oxidative Stress in Epilepsy.International journal of molecular sciences · 2017Review
- Dysregulation of zinc/lipid metabolism‑associated genes in the rat hippocampus and cerebral cortex in early adulthood following recurrent neonatal seizures.Molecular medicine reports · 2017Article
- Down-regulation of Pin1 in Temporal Lobe Epilepsy Patients and Mouse Model.Neurochemical research · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Neuronal cell death is a pathophysiological consequence of many brain insults that trigger epilepsy and has been implicated as a causal factor in epileptogenesis. Seizure-induced neuronal death features excitotoxic necrosis and apoptosis-associated signaling pathways, including activation of multiple members of the Bcl-2 gene family. The availability of mice in which individual Bcl-2 family members have been deleted has provided the means to determine whether they have causal roles in neuronal death and epileptogenesis in vivo. Studies show that multiple members of the Bcl-2 family are activated following status epilepticus and the seizure and damage phenotypes of eight different knockouts of the Bcl-2 family have now been characterized. Loss of certain pro-apoptotic members, including Puma, protected against seizure-induced neuronal death whereas loss of anti-apoptotic Mcl-1 and Bcl-w enhanced hippocampal damage. Notably, loss of two putatively pro-apoptotic members, Bak and Bmf, resulted in more seizure-damage while deletion of Bid had no effect, indicating the role of certain Bcl-2 family proteins in epileptic brain injury is distinct from their contributions following other stressors or in non-CNS tissue. Notably, Puma-deficient mice develop fewer spontaneous seizures after status epilepticus suggesting neuroprotection may preserve functional inhibition, either directly by preserving neuronal networks or indirectly, for example by limiting reactive gliosis and pro-inflammatory responses to neuronal death. Together, these studies support apoptosis-associated molecular mechanisms controlling neuronal death as a component of epileptogenesis which might be targetable to protect against seizure-damage, cognitive deficits and mitigate the severity of syndrome following epilepsy-precipitating injuries to the brain.
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