ReviewClinica chimica acta; international journal of clinical chemistry2015
Role of mitochondria in apoptotic and necroptotic cell death in the developing brain.
Review in Clinica chimica acta; international journal of clinical chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 99 citations in OpenAlex.
- Astrocyte autophagy-pyroptosis crosstalk in Alzheimer's: insights from knowledge graphs.BMC neurology · 2026Article
- Extrinsic apoptosis and necroptosis in telencephalic development: a single-cell mass cytometry study.Cell death and differentiation · 2026Article
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
- Pituitary adenylate cyclase-activating polypeptide and mitochondrial homeostasis in neuronal injury: mechanisms and translational prospects.Frontiers in immunology · 2026Review
- The Potential Clinical Relevance of Necrosis-Necroptosis Pathways for Hypoxic-Ischaemic Encephalopathy.Cells · 2025Review
- miRNA-105 Attenuates Hypoxic-Ischemic Brain Damage in Neonatal Rats by Inhibiting Apoptosis and Necroptosis.Neurochemical research · 2025Article
- The shifting landscape of the preterm brain.Neuron · 2025Review
- Review
- Erythronecroptosis: an overview of necroptosis or programmed necrosis in red blood cells.Molecular and cellular biochemistry · 2024Review
- Raloxifene Protects Oxygen-Glucose-Deprived Astrocyte Cells Used to Mimic Hypoxic-Ischemic Brain Injury.International journal of molecular sciences · 2024Article
- Impact of Exercise Training on Survival Rate and Neural Cell Death in Sepsis Through the Maintenance of Redox Equilibrium.International neurourology journal · 2024Article
- Neuroprotective Effects of Delayed TGF-β1 Receptor Antagonist Administration on Perinatal Hypoxic-Ischemic Brain Injury.Developmental neuroscience · 2024Article
- Early assessment of injury with optical markers in a piglet model of neonatal encephalopathy.Pediatric research · 2023Article
- Infantile Hypoxic Encephalopathy Mimicking Acute Encephalopathy with Biphasic Seizures and Late Reduced Diffusion (AESD) Identified as an Episode of Brief Resolved Unexplained Event (BRUE).Journal of clinical medicine · 2023Article
- Aluminum Induced Necroptosis of PC12 Cells via TNFR1-RIP1/RIP3 Signalling Pathway.Neurochemical research · 2022Article
- Mechanisms of Tertiary Neurodegeneration after Neonatal Hypoxic-Ischemic Brain Damage.Pediatric medicine (Hong Kong, China) · 2022Article
- Mitochondrial dynamics in the neonatal brain - a potential target following injury?Bioscience reports · 2022Review
- Preclinical Evidence for the Interplay between Oxidative Stress and RIP1-Dependent Cell Death in Neurodegeneration: State of the Art and Possible Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2021Review
- The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status.Journal of neuroinflammation · 2021Review
- Quality of Life and a Surveillant Endocannabinoid System.Frontiers in neuroscience · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hypoxic-ischemic encephalopathy induces secondary brain injury characterized by delayed energy failure. Currently, therapeutic hypothermia is the sole treatment available after severe intrapartum asphyxia in babies and acts to attenuate secondary loss of high energy phosphates improving both short- and long-term outcome. In order to develop the next generation of neuroprotective therapies, we urgently need to understand the underlying molecular mechanisms leading to cell death. Hypoxia-ischemia creates a toxic intracellular environment including accumulation of reactive oxygen/nitrosative species and intracellular calcium after the insult, inducing mitochondrial impairment. More specifically mitochondrial respiration is suppressed and calcium signaling is dysregulated. At a certain threshold, Bax-dependent mitochondrial permeabilization will occur leading to activation of caspase-dependent and apoptosis-inducing factor-dependent apoptotic cell death. In addition, hypoxia-ischemia induces inflammation, which leads to the release of TNF-α, TRAIL, TWEAK, FasL and Toll-like receptor agonists that will activate death receptors on neurons and oligodendroglia. Death receptors trigger apoptotic death via caspase-8 and necroptotic cell death through formation of the necrosome (composed of RIP1, RIP3 and MLKL), both of which converge at the mitochondria.
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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.