ReviewBiochimica et biophysica acta2010
Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia.
Review in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 2 of them syntheses 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
170 citing papers in PubMed, 2 syntheses or guidelines pooled it, 357 citations in OpenAlex.
- Microglia in Post-Traumatic Brain Injury (TBI) Cognitive Impairment: From Pathological Changes to Therapeutic Approaches.CNS neuroscience & therapeutics · 2025Pooled it
- Mechanisms of estrogens' dose-dependent neuroprotective and neurodamaging effects in experimental models of cerebral ischemia.International journal of molecular sciences · 2011Pooled it
- Modeling Hemorrhagic Shock in Male SD Rats by Fixed Volume Blood Withdrawal Followed by Partial Resuscitation and Long-Term Outcome Assessment.Medical sciences (Basel, Switzerland) · 2026Article
- Article
- Microglial mitochondria transfer to astrocytes via GPNMB-enriched extracellular vesicles alleviates cognitive deficits in tauopathy mice.Nature neuroscience · 2026Article
- Genistein Protects Against Lead-Induced Cognitive Impairment Through a Glutathione-Dependent Redox-Mitochondrial Apoptosis Axis.Molecules (Basel, Switzerland) · 2026Article
- Comprehensive Analysis of Immune-Related Mitochondrial Genes in Ischemic Stroke Through Integrated Bioinformatics and Validation.Biomedicines · 2026Article
- Targeting PKC/NF-κB/NLRP3-driven NcRNA neuroinflammatory crosstalk by condensed tannins in global cerebral ischemia.Inflammopharmacology · 2026Review
- Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress.Molecular neurobiology · 2026Article
- Article
- Endothelial glycocalyx shedding and oxidative stress in neuronal damage after return of spontaneous circulation in cardiac arrest.Scientific reports · 2025Article
- Mitochondrial Function, Oxidative Stress, Inflammation and Thrombolytic Treatment in Ischemic Stroke.International journal of molecular sciences · 2025Article
- Platelet Extracellular Vesicles as Natural Delivery Vehicles for Mitochondrial Dysfunction Therapy?ACS biomaterials science & engineering · 2025Review
- Chronic Administration with FAD012 (3,5-Dimethyl-4-hydroxycinnamic Acid) Maintains Cerebral Blood Flow and Ameliorates Swallowing Dysfunction After Chronic Cerebral Hypoperfusion in Rats.International journal of molecular sciences · 2025Article
- The E3-ligase Siah2 activates mitochondrial quality control in neurons to maintain energy metabolism during ischemic brain tolerance.Cell death & disease · 2025Article
- Article
- Mechanism of LCN2 in cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2025Review
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Induced neural stem cells ameliorate blood-brain barrier injury by modulating the calcium signaling pathway of astrocyte in cerebral ischemia-reperfusion rats.Frontiers in cell and developmental biology · 2025Article
- The role of reactive oxygen species in the regulation of the blood-brain barrier.Tissue barriers · 2025Review
110 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
8 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria play important roles as the powerhouse of the cell. After cerebral ischemia, mitochondria overproduce reactive oxygen species (ROS), which have been thoroughly studied with the use of superoxide dismutase transgenic or knockout animals. ROS directly damage lipids, proteins, and nucleic acids in the cell. Moreover, ROS activate various molecular signaling pathways. Apoptosis-related signals return to mitochondria, then mitochondria induce cell death through the release of pro-apoptotic proteins such as cytochrome c or apoptosis-inducing factor. Although the mechanisms of cell death after cerebral ischemia remain unclear, mitochondria obviously play a role by activating signaling pathways through ROS production and by regulating mitochondria-dependent apoptosis pathways.
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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.