ArticleFrontiers in cellular neuroscience2023
Loss of maturity and homeostatic functions in Tuberous Sclerosis Complex-derived astrocytes.
Article in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- TSC-associated microglial hyperactivity: enhanced calcium signaling, metabolism, and phagocytosis.Acta neuropathologica · 2026Article
- AAV hamartin gene therapy in a stochastic, cerebral mouse model of tuberous sclerosis type 1.Molecular therapy. Methods & clinical development · 2025Article
- Tumors and their microenvironments: Learning from pediatric brain pathologies.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Developmental neurotoxicity of bisphenol F and bisphenol S in animal model systems: A literature review.Neurotoxicology · 2025Review
- Physiological and Pathological Role of mTOR Signaling in Astrocytes.Neurochemical research · 2024Review
- WONOEP appraisal: The role of glial cells in focal malformations associated with early onset epilepsies.Epilepsia · 2024Review
- Single cell spatial biology over developmental time can decipher pediatric brain pathologies.Neurobiology of disease · 2024Review
- Astroglial calcium signaling and homeostasis in tuberous sclerosis complex.Acta neuropathologica · 2024Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Constitutive activation of the mTOR pathway, as observed in Tuberous Sclerosis Complex (TSC), leads to glial dysfunction and subsequent epileptogenesis. Although astrocytes are considered important mediators for synaptic clearance and phagocytosis, little is known on how astrocytes contribute to the epileptogenic network. Methods: We employed singlenuclei RNA sequencing and a hybrid fetal calf serum (FCS)/FCS-free cell culture model to explore the capacity of TSC-derived astrocytes to maintain glutamate homeostasis and clear debris in their environment. Results: We found that TSC astrocytes show reduced maturity on RNA and protein level as well as the inability to clear excess glutamate through the loss of both enzymes and transporters complementary to a reduction of phagocytic capabilities. Discussion: Our study provides evidence of mechanistic alterations in TSC astrocytes, underscoring the significant impairment of their supportive functions. These insights enhance our understanding of TSC pathophysiology and hold potential implications for future therapeutic interventions.
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Registered trials
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