Metabolic reprogramming of astrocytes in pathological conditions: implications for neurodegenerative diseases
Open accessAbstract
Astrocytes play a pivotal role in maintaining brain energy homeostasis, supporting neuronal function through glycolysis and lipid metabolism. This review explores the metabolic intricacies of astrocytes in both physiological and pathological conditions, highlighting their adaptive plasticity and diverse functions. Under normal conditions, astrocytes modulate synaptic activity, recycle neurotransmitters, and maintain the blood–brain barrier, ensuring a balanced energy supply and protection against oxidative stress. However, in response to central nervous system pathologies such as neurotrauma, stroke, infections, and neurodegenerative diseases like Alzheimer’s and Huntington’s disease, astrocytes undergo significant morphological, molecular, and metabolic changes. Reactive astrocytes upregulate glycolysis and fatty acid oxidation to meet increased energy demands, which can be protective in acute settings but may exacerbate chronic inflammation and disease progression. This review emphasizes the need for advanced molecular, genetic, and physiological tools to further understand astrocyte heterogeneity and their metabolic reprogramming in disease states.
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When driven into a reactive state by EDC-associated inflammation and oxidative stress, astrocytes can lose these homeostatic functions and instead sustain chronic inflammatory signaling, impair neurotransmitter clearance, and weaken neuronal metabolic support.
“When driven into a reactive state by EDC-associated inflammation and oxidative stress, however, astrocytes can lose these homeostatic functions and instead sustain chronic inflammatory signaling, impair neurotransmitter clearance, and weaken neuronal metabolic support (Calì et al., 2024; Khakh, 2025; Rupareliya et al., 2023).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Calì et al., 2024
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Experimental — accuracy not yet measuredUnder physiological conditions, astrocytes maintain BBB function, regulate extracellular ion balance, recycle neurotransmitters such as glutamate, provide metabolic support to neurons, and participate in synapse formation and elimination.
“Under physiological conditions, they maintain BBB function, regulate extracellular ion balance, recycle neurotransmitters such as glutamate, provide metabolic support to neurons, and participate in synapse formation and elimination.”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Calì et al., 2024
The Introduction (page not available) describes astrocytes’ role in BBB formation, uptake of excess potassium and glutamate, and metabolic support to neurons. It also says they modulate synaptic activity, but neither that passage nor the searched passages establish a role in both synapse formation and elimination. (LLM, conf=0.86)
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- Authors
- Calì, C., Cantando, I., Veloz Castillo, M. F., Gonzalez, L., & Bezzi, P.
- Affiliations
- Neuroscience Institute Cavalieri Ottolenghi (IT)
- University of Lausanne (CH)
- Department of Neuroscience “Rita Levi Montalcini”, University of Turin, 10124 Turin, Italy
- Sapienza University of Rome (IT)
- Corresponding author
- Calì, Corrado
- Bezzi, Paola
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2024-08-16
- Volume
- 25
- Issue
- 16
- Pages
- 8922
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC11354244
- OpenAlex
- W4401643850
- Cited by
- 66
- References
- 222
- Citations by year
- 2026: 44 · 2025: 21 · 2024: 1
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, cc-by)
- IRIS (submittedVersion, cc-by)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Funders
- Swiss National Science Foundation (SNSF) (310030_185363, GGP20037, 31NE30_204022, ECS00000036)
- telethon Italy (310030_185363, GGP20037, 31NE30_204022, ECS00000036)
- ERANET-Neuron SNSF (310030_185363, GGP20037, 31NE30_204022, ECS00000036)
- MUR–M4C2 1.5 of PNNR (310030_185363, GGP20037, 31NE30_204022, ECS00000036)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- astrocytes, brain energy homeostasis, glycolysis, fatty acid oxidation, reactive astrocytes, astrocyte heterogeneity, neurodegenerative diseases, Alzheimer's disease, Huntington's disease, stroke, neurotrauma, blood-brain barrier, oxidative stress, chronic inflammation, lipid metabolism
- MeSH terms
- Metabolic Reprogramming, Animals, Astrocytes, Energy Metabolism, Glycolysis, Humans, Neurodegenerative Diseases, Lipid Metabolism, Cellular Reprogramming
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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