Component

Mitochondrial delivery to lysosomes

Mitochondrial delivery to lysosomes

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. MMUT-deficient human kidney cells failed to show the control mt-Keima lysosomal shift after 24 hours of 5 micromolar rotenone.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Full text Results; Figures 2f,5c-f,6c-d
    experimental_model
    Urine-derived human mut0 MMA kidney tubular cells
    exposure
    MMUT-inactivating genotypes plus 5 micromolar rotenone for 24 hours
    limitations
    Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. mt-Keima is a delivery reporter.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    After experimental mitochondrial damage, these patient kidney cells delivered fewer mitochondria to lysosomes.
    primary_references
    [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    tissue_or_cell_type
    Kidney tubular cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1342–1354

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Urine-derived human mut0 MMA kidney tubular cells · source_derived_draft · unverified_draft

    ### mut0-kidney-impaired-mito-delivery MMUT-deficient human kidney cells failed to show the control mt-Keima lysosomal shift after 24 hours of 5 micromolar rotenone. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: After experimental mitochondrial damage, these patient kidney cells delivered fewer mitochondria to lysosomes. organism: Homo sapiens tissue_or_cell_type: Kidney tubular cells experimental_model: Urine-derived human mut0 MMA kidney tubular cells limitations: Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. mt-Keima is a delivery reporter. exposure: MMUT-inactivating genotypes plus 5 micromolar rotenone for 24 hours cross_nutrient: false evidence_location: Full text Results; Figures 2f,5c-f,6c-d [luciani-2020-mmut-mitophagy] Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency. (2020). https://pubmed.ncbi.nlm.nih.gov/32080200/ DOI: 10.1038/s41467-020-14729-8
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards