ReviewAntioxidants & redox signaling2011
Redox regulation of the intrinsic pathway in neuronal apoptosis.
Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- Microglia in Post-Traumatic Brain Injury (TBI) Cognitive Impairment: From Pathological Changes to Therapeutic Approaches.CNS neuroscience & therapeutics · 2025Pooled it
- Cell Death in Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Molecular Networks of Redox Dysregulation in Fetal Alcohol Spectrum Disorders: Mechanisms and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Comprehensive Analysis of Immune-Related Mitochondrial Genes in Ischemic Stroke Through Integrated Bioinformatics and Validation.Biomedicines · 2026Article
- Cisplatin as a Xenobiotic Agent: Molecular Mechanisms of Actions and Clinical Applications in Oncology.Journal of xenobiotics · 2026Review
- Recombinant HALT-1 induces mitochondrial-associated apoptotic mechanism in HeLa cells.Scientific reports · 2025Article
- Review
- UFBP1 Ameliorates Heat Stress-Induced Apoptosis via Mitochondria-Mediated Pathway in Bovine Mammary Epithelial Cells.Animals : an open access journal from MDPI · 2025Article
- Article
- Apoptosis signaling is activated as a transient pulse in neurons.Cell death and differentiation · 2025Article
- The E3-ligase Siah2 activates mitochondrial quality control in neurons to maintain energy metabolism during ischemic brain tolerance.Cell death & disease · 2025Article
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Article
- CKLF induces microglial activation via triggering defective mitophagy and mitochondrial dysfunction.Autophagy · 2024Article
- Carlos Gutiérrez-Merino: Synergy of Theory and Experimentation in Biological Membrane Research.Molecules (Basel, Switzerland) · 2024Review
- Carnosic Acid Shows Higher Neuroprotective Efficiency than Edaravone or Ebselen in In Vitro Models of Neuronal Cell Damage.Molecules (Basel, Switzerland) · 2023Article
- Evaluation of haematological, genotoxic, cytotoxic and ATR-FTIR alterations in blood cells of fish Channa punctatus after acute exposure of aniline.Scientific reports · 2023Article
- Disorders of Endogenous and Exogenous Antioxidants in Neurological Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- CaMKII and CaCell biology and toxicology · 2023Article
- Elevated ROS levels during the early development of Angelman syndrome alter the apoptotic capacity of the developing neural precursor cells.Molecular psychiatry · 2023Article
17 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
1 author at 1 institution in 1 country.
Funding
Abstract
Two principal pathways exist by which cells can undergo apoptotic death, known as the extrinsic and the intrinsic pathways. Binding of a ligand to a death receptor activates the extrinsic pathway. In the intrinsic pathway, an apoptotic stimulus, such as neurotrophin withdrawal or exposure to a toxin, causes a proapoptotic member of the Bcl-2 family of proteins, such as Bax, to permeabilize the outer mitochondrial membrane. This allows redistribution of cytochrome c from the mitochondrial intermembrane space into the cytoplasm, where it causes activation of caspase proteases and, subsequently, cell death. A dramatic increase occurs in mitochondria-derived reactive oxygen species (ROS) during the apoptotic death of sympathetic, cerebellar granule, and cortical neurons. These ROS lie downstream of Bax in each cell type. Here I review possible mechanisms by which Bax causes increased ROS during neuronal apoptosis. I also discuss evidence that these ROS are an important part of the apoptotic cascade in these cells. Finally, I discuss evidence that suggests that neurotrophins prevent release of cytochrome c in neurons through activation of an antioxidant pathway.
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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.