ArticleCell death & disease2012
Prevention of neonatal oxygen-induced brain damage by reduction of intrinsic apoptosis.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- A Novel Model for Simultaneous Evaluation of Hyperoxia-Mediated Brain and Lung Injury in Neonatal Rats.Cells · 2025Article
- Review
- GSDMD gene knockout alleviates hyperoxia-induced hippocampal brain injury in neonatal mice.Journal of neuroinflammation · 2023Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Systematic Review of the Therapeutic Role of Apoptotic Inhibitors in Neurodegeneration and Their Potential Use in Schizophrenia.Antioxidants (Basel, Switzerland) · 2022Review
- Perinatal Hyperoxia and Developmental Consequences on the Lung-Brain Axis.Oxidative medicine and cellular longevity · 2022Review
- Necrostatin-1 prolongs latency to convulsion in mice exposed to high oxygen partial pressure.Diving and hyperbaric medicine · 2021Article
- The Role of Caspase-2 in Regulating Cell Fate.Cells · 2020Review
- Current Evidence on Cell Death in Preterm Brain Injury in Human and Preclinical Models.Frontiers in cell and developmental biology · 2020Review
- Recombinant Slit2 attenuates neuronal apoptosis via the Robo1-srGAP1 pathway in a rat model of neonatal HIE.Neuropharmacology · 2019Article
- Adverse neuropsychiatric development following perinatal brain injury: from a preclinical perspective.Pediatric research · 2019Review
- Time Dependent Pathway Activation of Signalling Cascades in Rat Organs after Short-Term Hyperoxia.International journal of molecular sciences · 2018Article
- Anti-apoptotic effects of autophagy via ROS regulation in microtubule-targeted and PDGF-stimulated vascular smooth muscle cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
- Lung-Specific Extracellular Superoxide Dismutase Improves Cognition of Adult Mice Exposed to Neonatal Hyperoxia.Frontiers in medicine · 2018Article
- Protection of Oligodendrocytes Through Neuronal Overexpression of the Small GTPase Ras in Hyperoxia-Induced Neonatal Brain Injury.Frontiers in neurology · 2018Article
- [17β‑estradiol suppresses hyperoxia‑induced apoptosis of oligodendrocyte precursor cells through paired‑immunoglobulin‑like receptor B].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- Erythropoietin Restores Long-Term Neurocognitive Function Involving Mechanisms of Neuronal Plasticity in a Model of Hyperoxia-Induced Preterm Brain Injury.Oxidative medicine and cellular longevity · 2016Article
- Role of mitochondria in apoptotic and necroptotic cell death in the developing brain.Clinica chimica acta; international journal of clinical chemistry · 2015Review
- An Influence of Birth Weight, Gestational Age, and Apgar Score on Pattern Visual Evoked Potentials in Children with History of Prematurity.Neural plasticity · 2015Article
- Arginase 2 deficiency reduces hyperoxia-mediated retinal neurodegeneration through the regulation of polyamine metabolism.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Within the last decade, it became clear that oxygen contributes to the pathogenesis of neonatal brain damage, leading to neurocognitive impairment of prematurely born infants in later life. Recently, we have identified a critical role for receptor-mediated neuronal apoptosis in the immature rodent brain. However, the contribution of the intrinsic apoptotic pathway accompanied by activation of caspase-2 under hyperoxic conditions in the neonatal brain still remains elusive. Inhibition of caspases appears a promising strategy for neuroprotection. In order to assess the influence of specific caspases on the developing brain, we applied a recently developed pentapeptide-based group II caspase inhibitor (5-(2,6-difluoro-phenoxy)-3(R,S)-(2(S)-(2(S)-(3-methoxycarbonyl-2(S)-(3-methyl-2(S)-((quinoline-2-carbonyl)-amino)-butyrylamino)propionylamino)3-methylbutyrylamino)propionylamino)-4-oxo-pentanoic acid methyl ester; TRP601). Here, we report that elevated oxygen (hyperoxia) triggers a marked increase in active caspase-2 expression, resulting in an initiation of the intrinsic apoptotic pathway with upregulation of key proteins, namely, cytochrome c, apoptosis protease-activating factor-1, and the caspase-independent protein apoptosis-inducing factor, whereas BH3-interacting domain death agonist and the anti-apoptotic protein B-cell lymphoma-2 are downregulated. These results coincide with an upregulation of caspase-3 activity and marked neurodegeneration. However, single treatment with TRP601 at the beginning of hyperoxia reversed the detrimental effects in this model. Hyperoxia-mediated neurodegeneration is supported by intrinsic apoptosis, suggesting that the development of highly selective caspase inhibitors will represent a potential useful therapeutic strategy in prematurely born infants.
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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.