ReviewFrontiers in cellular neuroscience2017
Cell Death in the Developing Brain after Hypoxia-Ischemia.
Review in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed.
- Selective non-nuclear estrogen receptor activation with PaPE-1 evokes neuroprotection involving mTOR/MEK in an in vitro model of hypoxic/ischemic injury.Pharmacological reports : PR · 2026Article
- High-Altitude Hypoxia Activates JNK-p53 Signaling: Linking Hippocampal Energy Crisis to Cognitive Impairment.CNS neuroscience & therapeutics · 2026Article
- TRPM7 kinase inhibitor TG100-115 provides neuroprotection against neonatal hypoxic-ischemic brain injury.Acta pharmacologica Sinica · 2026Article
- Review
- SP1 Aggravates Neonatal Hypoxic-Ischemic Brain Damage by Promoting Ferroptosis Through Transcriptional Upregulation of ACSL4.ASN neuro · 2026Article
- Delayed necrostatin-1s infusion attenuates cystic white matter injury in preterm fetal sheep.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- The Potential Clinical Relevance of Necrosis-Necroptosis Pathways for Hypoxic-Ischaemic Encephalopathy.Cells · 2025Review
- Does the Maternal Gut Microbiome Influence the Outcome of Perinatal Asphyxia?Antioxidants (Basel, Switzerland) · 2025Review
- What are the implications of sex differences in cell death for treatment after neonatal hypoxia-ischemia, if any?Pediatric research · 2025Article
- Preconditioning and Posttreatment Strategies in Neonatal Hypoxic-Ischemic Encephalopathy: Recent Advances and Clinical Challenges.Molecular neurobiology · 2025Review
- Review
- 50 years of methylprednisolone application in spinal cord injury: a bibliometric analysis.Acta neurochirurgica · 2025Review
- Traditional and non-traditional behavioral tests demonstrate the attenuation of cognitive deficits by therapeutic hypothermia in a rat model of neonatal hypoxic-ischemic encephalopathy.Frontiers in behavioral neuroscience · 2025Article
- Berberine and its derivatives: mechanisms of action in myocardial vascular endothelial injury - a review.Frontiers in pharmacology · 2025Review
- Heat Hardening Ameliorates Apoptotic and Inflammatory Effects Through Increased Autophagy in Mussels.Marine biotechnology (New York, N.Y.) · 2024Article
- Hydrogen alleviates hypoxic-ischaemic brain damage in neonatal rats by inhibiting injury of brain pericytes.Journal of cellular and molecular medicine · 2024Article
- Regulated cell death in hypoxic-ischaemic encephalopathy: recent development and mechanistic overview.Cell death discovery · 2024Review
- Association between decreased cord blood inter-alpha inhibitor levels and neonatal encephalopathy at birth.Early human development · 2024Article
- Hypoxia in the Blue MusselGenes · 2024Article
- Neuroprotective Effects of Delayed TGF-β1 Receptor Antagonist Administration on Perinatal Hypoxic-Ischemic Brain Injury.Developmental neuroscience · 2024Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perinatal insults such as hypoxia-ischemia induces secondary brain injury. In order to develop the next generation of neuroprotective therapies, we urgently need to understand the underlying molecular mechanisms leading to cell death. The cell death mechanisms have been shown to be quite different in the developing brain compared to that in the adult. The aim of this review is update on what cell death mechanisms that are operating particularly in the setting of the developing CNS. In response to mild stress stimuli a number of compensatory mechanisms will be activated, most often leading to cell survival. Moderate-to-severe insults trigger regulated cell death. Depending on several factors such as the metabolic situation, cell type, nature of the stress stimulus, and which intracellular organelle(s) are affected, the cell undergoes apoptosis (caspase activation) triggered by BAX dependent mitochondrial permeabilzation, necroptosis (mixed lineage kinase domain-like activation), necrosis (via opening of the mitochondrial permeability transition pore), autophagic cell death (autophagy/Na
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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.