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Cited by 318Cell death mechanisms and regulationAcute Ischemic Stroke ManagementNeuroprotection in Cerebral Ischemia

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

Mattson, Mark P., Culmsee, Carsten, Yu, Zai Fang·2000·Cell and Tissue Research
DOI 10.1007/s004419900154
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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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Crossref · 10.1007/s004419900154

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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.
ORCID
Venue
Cell and Tissue Research
Publisher
Springer Science and Business Media LLC
Published
2000-03-23
Volume
301
Issue
1
Pages
173-187
ISSN
  • 0302-766X (ISSN-L)
  • 1432-0878
DOI
10.1007/s004419900154
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

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