ArticleScientific reports2025
Deficiency in NPC2 results in disruption of mitochondria-late endosome/lysosomes contact sites and endo-lysosomal lipid dyshomeostasis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- HKDC1 contributes to aberrant lysosome-mitochondria contact in Niemann-Pick disease type C.bioRxiv : the preprint server for biology · 2026Article
- Organelle contact sites in cancer cells.Cell death & disease · 2026Review
- Constraint-based modelling of metabolic dysregulation in Gaucher disease: mitochondrial dysfunction and disrupted cholesterol homeostasis.Orphanet journal of rare diseases · 2026Article
- Risk prediction and therapeutic targets for incident pulmonary hypertension: a large-scale proteomic profiling and Mendelian randomization study.Frontiers of medicine · 2025Article
- Proteomics mediates the effects of biological aging on the progression of cardio-renal-metabolic comorbidity: a UK biobank cohort study.Cardiovascular diabetology · 2025Article
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6 authors.
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Abstract
Dysfunction of the endo-lysosomal intracellular Cholesterol transporter 2 protein (NPC2) leads to the onset of Niemann-Pick Disease Type C (NPC), a lysosomal storage disorder. Metabolic and homeostatic mechanisms are disrupted in lysosomal storage disorders (LSDs) hence we characterized a cellular model of NPC2 knock out, to assess alterations in organellar function and inter-organellar crosstalk between mitochondria and lysosomes. We performed characterization of lipid alterations and confirmed altered lysosomal morphology, but no overt changes in oxidative stress markers. Using several techniques, we demonstrated that contacts between mitochondria and late endosomes/lysosomes are reduced in NPC2
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