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

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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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Background
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Authors: Dienel, G. A., & Hertz, L.
Affiliations: University of Arkansas for Medical Sciences (US)
China Medical University (CN)
Corresponding author: Dienel, Gerald A.
ORCID: Dienel, Gerald A.
Hertz, Leif
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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