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Cited by 150Neuroprotection in Cerebral IschemiaNeuroscience and Neuropharmacology ResearchAcute Ischemic Stroke Management

The DOI matches its Crossref record; 324 of the 331 references it cites were found in a registry or an index.

Astrocytic contributions to bioenergetics of cerebral ischemia

Dienel, Gerald A., Hertz, Leif·2005·Glia
DOI 10.1002/glia.20157
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Abstract

Astrocytes are multifunctional cells that interact with neurons and other astrocytes in signaling and metabolic functions, and their resistance to pathophysiological conditions can help restrict loss of tissue after an ischemic event provided adequate nutrients are supplied to support their requirements. Astrocytes have substantial oxidative capacity and mechanisms to upregulate glycolytic capability when respiration is impaired. An astrocytic enzyme that synthesizes a powerful activator of glycolysis is not present in neurons, endowing astrocytes with the ability to sustain ATP production under restrictive conditions. The monocarboxylic acid transporter (MCT) isoforms predominating in astrocytes are optimized to facilitate very large increases in lactate flux as lactate concentration increases within (1-3 mM) and above (>3 mM) the normal range. In sharp contrast, the major neuronal MCT serves as a barrier to increased transmembrane transport as lactate rises above 1 mM, restricting both entry and efflux. Lactate can serve as fuel during recovery from ischemia but direct evidence that lactate is oxidized by neurons (vs. astrocytes) to maintain synaptic function is lacking. Astrocytes have critical roles in regulation of ionic homeostasis and control of extracellular glutamate levels, and spreading depression associated with ischemia places high demands on energy supplies in astrocytes and contributes to metabolic exhaustion and demise. Disruption of Ca2+ homeostasis, generation of oxygen free radicals and nitric oxide, and mitochondrial depolarization contribute to astrocyte death during and after a metabolic insult. Novel pharmaceutical agents targeted to astrocytes and hyperoxic therapy that restores penumbral oxygen level during energy failure might improve postischemic outcome.

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Crossref · 10.1002/glia.20157

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324 of 324 references verified0 citation errors · 0 not checkable

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7 of the 331 references couldn’t be matched to a known paper.

Research works printed but not linked: 19

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Metadata

Authors
Dienel, G. A., & Hertz, L.
Affiliations
  • University of Arkansas for Medical Sciences (US)
  • China Medical University (CN)
Corresponding author
Dienel, Gerald A.
ORCID
Venue
Glia
Publisher
Wiley
Published
2005-04-21
Volume
50
Issue
4
Pages
362-388
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
DOI
10.1002/glia.20157
OpenAlex
W1964844927
Cited by
150
References
331
Citations by year
2026: 2 · 2025: 6 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 6 · 2019: 3 · 2018: 7 · 2017: 8 · 2016: 4 · 2015: 6 · 2014: 7 · 2013: 10 · 2012: 10
FWCI
1.21
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Neurological Disorders and Stroke (NS 36728, R01NS036728, NS38230)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
Keywords
astrocytes, cerebral ischemia, glycolysis, lactate transport, monocarboxylate transporters, lactate oxidation, cortical spreading depression, ion homeostasis, extracellular glutamate, calcium homeostasis, mitochondrial depolarization, reactive oxygen species, nitric oxide, penumbra, neuroprotection
MeSH terms
Animals, Astrocytes, Cell Survival, Brain Ischemia, Energy Metabolism, Humans

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