The DOI matches its Crossref record; 121 of the 121 references it cites were found in a registry or an index.
Apoptotic and antiapoptotic mechanisms in stroke
Abstract
Apoptosis is a form of programmed cell death that occurs in neurons during development of the nervous system and may also be a prominent form of neuronal death in chronic neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. Recent findings also implicate apoptosis in neuronal degeneration after ischemic brain injury in animal models of stroke. Activation of both apoptotic and antiapoptotic signaling cascades occurs in neurons in animal and cell culture models of stroke. Apoptotic cascades involve: increased levels of intracellular oxyradicals and calcium; induction of expression of proteins such as Par-4 (prostate apoptosis response-4), which act by promoting mitochondrial dysfunction and suppressing antiapoptotic mechanisms; mitochondrial membrane depolarization, calcium uptake, and release of factors (e.g., cytochrome c) that ultimately induce nuclear DNA condensation and fragmentation; activation of cysteine proteases of the caspase family; activation of transcription factors such as AP-1 that may induce expression of "killer genes." Antiapoptotic signaling pathways are activated by neurotrophic factors, certain cytokines, and increases in oxidative and metabolic stress. Such protective pathways include: activation of the transcription factors (e.g., nuclear factor-kappa B, NF-kappa B) that induce expression of stress proteins, antioxidant enzymes, and calcium-regulating proteins; phosphorylation-mediated modulation of ion channels and membrane transporters; cytoskeletal alterations that modulate calcium homeostasis; and modulation of proteins that stabilize mitochondrial function (e.g., Bcl-2). Intervention studies in experimental stroke models have identified a battery of approaches of potential benefit in reducing neuronal death in stroke patients, including administration of antioxidants, calcium-stabilizing agents, caspase inhibitors, and agents that activate NF-kappa B. Interestingly, recent studies suggest novel dietary approaches (e.g., food restriction and supplementation with antioxidants) that may reduce brain damage following stroke.
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“Focal cerebral ischemia by middle cerebral artery occlusion (MCAo) induces apoptotic neural cell death that is primarily localized to the area immediately adjacent to the infarcted tissue, known as the ischemic boundary zone (IBZ) [1].”
From MicroRNA‐21 protects neurons from ischemic death (2010) · cites this paper as [1]
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Metadata
- Authors
- Mattson, M. P., Culmsee, C., & Yu, Z. F.
- Affiliations
- National Institute on Aging (US)
- Corresponding author
- Mattson, Mark P.
- Venue
- Cell and Tissue Research
- Published
- 2000-03-23
- Volume
- 301
- Issue
- 1
- Pages
- 173-187
- ISSN
- 0302-766X (ISSN-L)
- 1432-0878
- OpenAlex
- W2147278993
- Cited by
- 318
- References
- 121
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 7 · 2023: 6 · 2022: 5 · 2021: 10 · 2020: 4 · 2019: 4 · 2018: 8 · 2017: 9 · 2016: 5 · 2015: 7 · 2014: 16 · 2013: 9 · 2012: 16
- FWCI
- 7.48
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell and Tissue Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Keywords
- apoptosis, stroke, ischemic brain injury, neuronal cell death, anti-apoptotic signaling, mitochondrial dysfunction, caspases, cytochrome c release, NF-κB, Bcl-2, neurotrophic factors, oxidative stress, calcium homeostasis, antioxidants, caspase inhibitors, dietary restriction, dietary supplementation
- MeSH terms
- Animals, Brain, Calcium, Carrier Proteins, Cell Nucleus, Brain Ischemia, Humans, Mitochondria, Models, Biological, Nerve Growth Factors, Neurons, Signal Transduction, Gene Expression, Cytokines, Apoptosis, Reactive Oxygen Species, Stroke, Intracellular Signaling Peptides and Proteins, Apoptosis Regulatory Proteins, Mice, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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