ArticleJournal of neuroinflammation2024
mTOR activation induces endolysosomal remodeling and nonclassical secretion of IL-32 via exosomes in inflammatory reactive astrocytes.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The dual role of mTOR in multiple sclerosis pathophysiology: a systematic review.Journal of neurology · 2026Pooled it
- CRISPR and Myelin regeneration: a systematic review of applications in demyelinating CNS Disorders, with a focus on MS.Regenerative medicine · 2025Pooled it
- Article
- Integrated Characterization of ceRNA (circRNA/lncRNA/miRNA/mRNA) Regulatory Networks in aAnimals : an open access journal from MDPI · 2026Article
- Dysregulation of exosomal miRNAs in A2 astrocytes under oxygen-glucose deprivation is associated with neuronal pyroptosis: a role for miR-139-5p in targeting NLRP3.Journal of orthopaedic surgery and research · 2026Article
- The Dual Role of Glial Extracellular Vesicles in Neurodegeneration: Insights from iPSC-Based Models.International journal of molecular sciences · 2026Review
- Targeting MAPK-dependent pathways to modulate reactive astrocyte pathology in neurodegeneration.Communications biology · 2026Article
- Neuroinflammation-induced downregulation of RAB7 in murine astrocytes disrupts endo-lysosomal homeostasis and induces astrogliosis.Cell communication and signaling : CCS · 2026Article
- Spatial transcriptomics identifies IL-32 as a lipid droplet-associated cytokine linked to tubular injury in human diabetic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Senescent Astrocytes: A New Player in Brain Aging and Cognitive Decline.Brain sciences · 2026Review
- Tiny Messengers, Huge Consequences: Extracellular Vesicles and mTOR Signaling in Neuroinflammation.Journal of neurochemistry · 2025Review
- Glial phagocytosis for synapse and toxic proteins in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- Lysosomal acidification impairment in astrocyte-mediated neuroinflammation.Journal of neuroinflammation · 2025Review
- The Role of Small Extracellular Vesicles Derived from Glial Cells in the Central Nervous System under both Normal and Pathological Conditions.Neurochemical research · 2025Review
- Astrocytes in Primary Familial Brain Calcification (PFBC): Emphasis on the Importance of Induced Pluripotent Stem Cell-Derived Human Astrocyte Models.Advances in experimental medicine and biology · 2025Review
- Targeting autophagy in astrocytes: a potential for neurodegenerative disease intervention.Frontiers in cellular neuroscience · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Astrocytes respond and contribute to neuroinflammation by adopting inflammatory reactive states. Although recent efforts have characterized the gene expression signatures associated with these reactive states, the cell biology underlying inflammatory reactive astrocyte phenotypes remains under-explored. Here, we used CRISPR-based screening in human iPSC-derived astrocytes to identify mTOR activation a driver of cytokine-induced endolysosomal system remodeling, manifesting as alkalinization of endolysosomal compartments, decreased autophagic flux, and increased exocytosis of certain endolysosomal cargos. Through endolysosomal proteomics, we identified and focused on one such cargo-IL-32, a disease-associated pro-inflammatory cytokine not present in rodents, whose secretion mechanism is not well understood. We found that IL-32 was partially secreted in extracellular vesicles likely to be exosomes. Furthermore, we found that IL-32 was involved in the polarization of inflammatory reactive astrocyte states and was upregulated in astrocytes in multiple sclerosis lesions. We believe that our results advance our understanding of cell biological pathways underlying inflammatory reactive astrocyte phenotypes and identify potential therapeutic targets.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.