Component
Caspase-9 / CASP9
Initiator caspase of the mitochondrial apoptotic pathway, measured in phosphate-exposed hypertrophic chondrocytes.
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 acts on it
Phosphate exposure activated the caspase-9-dependent mitochondrial apoptotic pathway in cultured primary mouse hypertrophic chondrocytes.
Experimental context and source evidence
- cross_nutrient
- Vitamin D–calcium–phosphate regulation.
- evidence_locator
- Primary abstract and opening experimental-results summary; web-assay-excerpts.json
- evidence_scope
- D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.
- experimental_model
- Primary mouse chondrocytes; caspase-9 pathway and apoptosis assays
- exposure
- Inorganic phosphate exposure in differentiated primary cultures; exact dose/time not recovered in the primary passages used.
- limitations
- Cell differentiation and exposure conditions matter; no nutrient dose recommendation, universal phosphate sensor or human serum threshold is established.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Mus musculus
- plain_language
- Phosphate served as a signal for a cartilage-cell maturation pathway in this culture system.
- primary_references
- [vdm-sabbagh2005] Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. (2005). https://pubmed.ncbi.nlm.nih.gov/15976027/ DOI: 10.1073/pnas.0502249102
- tissue_or_cell_type
- Cultured hypertrophic chondrocytes
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 793–807
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary mouse chondrocytes; caspase-9 pathway and apoptosis assays · source_derived_draft · unverified_draft
### vdm-phosphate-activates-chondrocyte-caspase9 Phosphate exposure activated the caspase-9-dependent mitochondrial apoptotic pathway in cultured primary mouse hypertrophic chondrocytes. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphate served as a signal for a cartilage-cell maturation pathway in this culture system. organism: Mus musculus tissue_or_cell_type: Cultured hypertrophic chondrocytes experimental_model: Primary mouse chondrocytes; caspase-9 pathway and apoptosis assays limitations: Cell differentiation and exposure conditions matter; no nutrient dose recommendation, universal phosphate sensor or human serum threshold is established. exposure: Inorganic phosphate exposure in differentiated primary cultures; exact dose/time not recovered in the primary passages used. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Primary abstract and opening experimental-results summary; web-assay-excerpts.json nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-sabbagh2005] Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. (2005). https://pubmed.ncbi.nlm.nih.gov/15976027/ DOI: 10.1073/pnas.0502249102
Complete structured claim and evidence
Where it participates (unsigned role)
Treatment of U251 glioma cells with capsaicin and dihydrocapsaicin resulted in a dose- and time-dependent inhibition of cell viability and induction of apoptosis, whereas few effects were observed on the viability of L929 normal murine fibroblast cells, and the apoptosis was associated with generation of reactive oxygen species, increased calcium concentrations, mitochondrial depolarization, release of cytochrome c into the cytosol and activation of caspase-9 and caspase-3, with anti-tumour effects confirmed in a murine tumour xenograft model.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dihydrocapsaicin-research/27748914.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90", "start_char": 0, "end_char": 1610, "text_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90"}
- experimental_model
- U251 human glioma cells with flow cytometry, transmission electron microscopy and a murine xenograft model
- exposure
- Capsaicin and dihydrocapsaicin applied across doses and times, with L929 normal fibroblasts as a selectivity control
- limitations
- Includes a normal-cell control and an in vivo arm. Cell-line concentrations are not stated in the abstract and are not assumed here.
- nutrient_topic
- Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
- organism
- Human cells and mouse
- plain_language
- It kills glioma cells through the mitochondria while largely sparing normal cells.
- primary_references
- [dhc-p27748914] Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+‑mediated mitochondrial pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27748914/ DOI: 10.3892/mmr.2016.5784
- tissue_or_cell_type
- Glioma cells
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · U251 human glioma cells with flow cytometry, transmission electron microscopy and a murine xenograft model · source_derived_draft · unverified_draft
### dhc-glioma-apoptosis Treatment of U251 glioma cells with capsaicin and dihydrocapsaicin resulted in a dose- and time-dependent inhibition of cell viability and induction of apoptosis, whereas few effects were observed on the viability of L929 normal murine fibroblast cells, and the apoptosis was associated with generation of reactive oxygen species, increased calcium concentrations, mitochondrial depolarization, release of cytochrome c into the cytosol and activation of caspase-9 and caspase-3, with anti-tumour effects confirmed in a murine tumour xenograft model. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: It kills glioma cells through the mitochondria while largely sparing normal cells. organism: Human cells and mouse tissue_or_cell_type: Glioma cells experimental_model: U251 human glioma cells with flow cytometry, transmission electron microscopy and a murine xenograft model limitations: Includes a normal-cell control and an in vivo arm. Cell-line concentrations are not stated in the abstract and are not assumed here. exposure: Capsaicin and dihydrocapsaicin applied across doses and times, with L929 normal fibroblasts as a selectivity control evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/27748914.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90", "start_char": 0, "end_char": 1610, "text_sha256": "ffc172fb64714099772462ba33304b69637efac75f1f218f2032e26bbc32dc90"} [dhc-p27748914] Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+‑mediated mitochondrial pathway. (2016). https://pubmed.ncbi.nlm.nih.gov/27748914/ DOI: 10.3892/mmr.2016.5784
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.