ArticleNeurology research international2012
Hypoxic-ischemic injury in the developing brain: the role of reactive oxygen species originating in mitochondria.
Article in Neurology research international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 102 citations in OpenAlex.
- Targeting the mitochondrial thermogenesis pathway for neuroprotection in neonatal hypoxic-ischemic encephalopathy by curcumin.Acta pharmacologica Sinica · 2026Article
- Natural History of Alternating Hemiplegia of Childhood: Vulnerabilities in Early Childhood and Predictive Factors for Long-Term Outcomes.Annals of the Child Neurology Society · 2025Article
- Preconditioning and Posttreatment Strategies in Neonatal Hypoxic-Ischemic Encephalopathy: Recent Advances and Clinical Challenges.Molecular neurobiology · 2025Review
- Proteomic analysis of whole blood to investigate the therapeutic effects of nervonic acid on cerebral ischemia-reperfusion injury in rats.Frontiers in cell and developmental biology · 2025Article
- Research progress of propofol in alleviating cerebral ischemia/reperfusion injury.Pharmacological reports : PR · 2024Review
- Caffeine: The Story beyond Oxygen-Induced Lung and Brain Injury in Neonatal Animal Models-A Narrative Review.Antioxidants (Basel, Switzerland) · 2024Review
- Effect of dimethyl fumarate on mitochondrial metabolism in a pediatric porcine model of asphyxia-induced in-hospital cardiac arrest.Scientific reports · 2024Article
- Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Six Functions of Respiration: Isn't It Time to Take Control over ROS Production in Mitochondria, and Aging Along with It?International journal of molecular sciences · 2023Review
- Effects of Three Different Doses of Inter-Alpha Inhibitor Proteins on Severe Hypoxia-Ischemia-Related Brain Injury in Neonatal Rats.International journal of molecular sciences · 2022Article
- Correlation of Cerebral Microdialysis with Non-Invasive Diffuse Optical Cerebral Hemodynamic Monitoring during Deep Hypothermic Cardiopulmonary Bypass.Metabolites · 2022Article
- Effect of expansion of human umbilical cord blood CD34 + cells on neurotrophic and angiogenic factor expression and function.Cell and tissue research · 2022Article
- Article
- Inter-alpha Inhibitor Proteins Ameliorate Brain Injury and Improve Behavioral Outcomes in a Sex-Dependent Manner After Exposure to Neonatal Hypoxia Ischemia in Newborn and Young Adult Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Revealing the Impact of Mitochondrial Fitness During Early Neural Development Using Human Brain Organoids.Frontiers in molecular neuroscience · 2022Review
- Neuroprotective strategies of cerebrolysin for the treatment of infants with neonatal hypoxic-ischemic encephalopathy.Acta neurologica Belgica · 2021Review
- Oxidative stress battles neuronal Bcl-xL in a fight to the death.Neural regeneration research · 2021Article
- Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases.Frontiers in endocrinology · 2021Review
- Novel Neuroprotective Agents to Treat Neonatal Hypoxic-Ischemic Encephalopathy: Inter-Alpha Inhibitor Proteins.International journal of molecular sciences · 2020Review
- Phenolic Acids-Rich Fractions fromMolecules (Basel, Switzerland) · 2020Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction is the most fundamental mechanism of cell damage in cerebral hypoxia-ischemia and reperfusion. Mitochondrial respiratory chain (MRC) is increasingly recognized as a source for reactive oxygen species (ROS) in the postischemic tissue. Potentially, ROS originating in MRC can contribute to the reperfusion-driven oxidative stress, promoting mitochondrial membrane permeabilization. The loss of mitochondrial membranes integrity during reperfusion is considered as the major mechanism of secondary energy failure. This paper focuses on current data that support a pathogenic role of ROS originating from mitochondrial respiratory chain in the promotion of secondary energy failure and proposes potential therapeutic strategy against reperfusion-driven oxidative stress following hypoxia-ischemia-reperfusion injury of the developing brain.
Identifiers
What OpenQuestion holds
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.