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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Cites
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Bcl-2 functions in an antioxidant pathway to prevent apoptosis
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Mitochondrial control of apoptosis
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Role of Oxidants in Ischemic Brain Damage
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Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications
Brann, D. W., Dhandapani, K. M., Wakade, C. G., Mahesh, V. B., & Khan, M. M. (2007) · Steroids · doi:10.1016/j.steroids.2007.02.003 · Cited by 677
Pathophysiology, treatment, and animal and cellular models of human ischemic stroke
Woodruff, T., Thundyil, J., Tang, S.-C., Sobey, C., Taylor, S., & Arumugam, T. (2011) · Molecular Neurodegeneration · doi:10.1186/1750-1326-6-11 · Cited by 594
Oxidants, antioxidants and the ischemic brain
Warner, D. S., Sheng, H., & Batinic̈‐Haberle, I. (2004) · Journal of Experimental Biology · doi:10.1242/jeb.01022 · Cited by 598
Almeida, R. D., Manadas, B. J., Melo, C. V., Gomes, J. R., Mendes, C. S., Grãos, M., Carvalho, R. F., Carvalho, A. P., & Duarte, C. B. (2005) · Cell Death and Differentiation · doi:10.1038/sj.cdd.4401662 · Cited by 592
Non-invasive detection of apoptosis using magnetic resonance imaging and a targeted contrast agent
Zhao, M. F., Beauregard, D. A., Loizou, L., Davletov, B. A., & Brindle, K. M. (2001) · Nature Medicine · doi:10.1038/nm1101-1241 · Cited by 524
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
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