ArticleNature communications2024
NPC1 links cholesterol trafficking to microglial morphology via the gastrosome.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Lack of cathepsin B increases severity in Niemann-Pick disease, type C1 mice.Neuroscience letters · 2026Article
- NPC1 deficiency engages a lysosome-genome-immune program linked to neurodegeneration and cellular aging signatures.bioRxiv : the preprint server for biology · 2026Article
- A scalable human-zebrafish xenotransplantation model reveals gastrosome-mediated processing of dying neurons by human microglia.Communications biology · 2026Article
- Heterogeneity in lysosomal dynamics and metabolic functions along the kidney proximal tubule.Nature communications · 2026Article
- The SLC-ome of membrane transport: From molecular discovery to physiology and clinical applications.Physiological reviews · 2025Review
- NPC1 as a novel therapeutic target for induction of pyroptosis in cancers.Biomarker research · 2025Article
- Autophagy-NADFrontiers in molecular biosciences · 2025Review
- Interpretable machine learning for predicting 30-day mortality following intracranial hemorrhage surgery.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Microglia play important roles in brain development and homeostasis by removing dying neurons through efferocytosis. Morphological changes in microglia are hallmarks of many neurodegenerative conditions, such as Niemann-Pick disease type C. Here, NPC1 loss causes microglia to shift from a branched to an ameboid form, though the cellular basis and functional impact of this change remain unclear. Using zebrafish, we show that NPC1 deficiency causes an efferocytosis-dependent expansion of the microglial gastrosome, a collection point for engulfed material. In vivo and in vitro experiments on microglia and mammalian macrophages demonstrate that NPC1 localizes to the gastrosome, and its absence leads to cholesterol accumulation in this compartment. NPC1 loss and neuronal cell death synergistically affect gastrosome size and cell shape, increasing the sensitivity of NPC1-deficient cells to neuronal cell death. Finally, we demonstrate conservation of cholesterol accumulation and gastrosome expansion in NPC patient-derived fibroblasts, offering an interesting target for further disease investigation.
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Registered trials
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