Component
Human PINK1 kinase
Human PINK1 kinase
2 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Adenoviral human PINK1 expression restored Parkin recruitment in MMUT-deficient human kidney tubular cells.
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
- HA-PINK1 adenovirus versus empty-vector control
- limitations
- Inherited MMUT machinery defect; cannot be generalized to nutritional B12 deficiency or neurons. Gene-delivery rescue is not an established clinical therapy.
- nutrient_topic
- Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
- organism
- Homo sapiens
- plain_language
- Adding PINK1 restored mitochondrial marking in this patient-cell model.
- 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 1370–1382
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
### pink1-restores-parkin-mmut-kidney Adenoviral human PINK1 expression restored Parkin recruitment in MMUT-deficient human kidney tubular cells. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding PINK1 restored mitochondrial marking in this patient-cell model. 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. Gene-delivery rescue is not an established clinical therapy. exposure: HA-PINK1 adenovirus versus empty-vector control 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
Where it participates (unsigned role)
Compound C blocked hydroxytyrosol-associated PINK1 mitophagy in zebrafish liver cells, and cyclosporine blocked the measured mitochondrial benefits.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- dose
- Hydroxytyrosol with compound C or cyclosporine
- duration
- Cell assay accompanying fish feeding
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- Zebrafish liver cell line with an eight-week spotted-seabass feeding arm
- limitations
- This fish/cell mechanism is not direct evidence for human liver disease or a clinical drug interaction.
- nutrient_topic
- Hydroxytyrosol chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Hydroxytyrosol
- organism
- Zebrafish liver cell line with an eight-week spotted-seabass feeding arm
- plain_language
- Compound C blocked hydroxytyrosol-associated PINK1 mitophagy in zebrafish liver cells, and cyclosporine blocked the measured mitochondrial benefits.
- primary_references
- Hydroxytyrosol Promotes the Mitochondrial Function through Activating Mitophagy. (2022). https://pubmed.ncbi.nlm.nih.gov/35624756/ DOI: 10.3390/antiox11050893
- route
- In vitro perturbation
- tissue
- AMPK/PINK1 mitophagy and mitochondrial function
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Hydroxytyrosol: mechanism of action and interactions (2026-09-20) · lines 121–130
Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Zebrafish liver cell line with an eight-week spotted-seabass feeding arm · source_derived_draft · unverified_draft
## hydroxytyrosol-ampk-pink1-mitophagy Compound C blocked hydroxytyrosol-associated PINK1 mitophagy in zebrafish liver cells, and cyclosporine blocked the measured mitochondrial benefits. Model/species: Zebrafish liver cell line with an eight-week spotted-seabass feeding arm Tissue/system: AMPK/PINK1 mitophagy and mitochondrial function Exposure: Hydroxytyrosol with compound C or cyclosporine Route: In vitro perturbation Duration: Cell assay accompanying fish feeding Limits: This fish/cell mechanism is not direct evidence for human liver disease or a clinical drug interaction. Primary reference: Hydroxytyrosol Promotes the Mitochondrial Function through Activating Mitophagy. (2022). https://pubmed.ncbi.nlm.nih.gov/35624756/ DOI: 10.3390/antiox11050893 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.