Component

Dermal fibroblast

Dermal fibroblast. Species, exposure and limitations are retained in each linked claim.

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

Read recorded mechanisms Open recursive mind map

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

Where it participates (unsigned role)

  1. A one-hour exposure at oxygen pressures between 106 and 300 kPa increased proliferation of both normal and diabetic fibroblasts, with a dose-dependent peak at 250 kPa for normal and 200 kPa for diabetic cells, and the effects were not due to hydrostatic pressure per se.

    Hyperbaric oxygen therapy → Human fibroblast proliferation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/16984424.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a", "start_char": 0, "end_char": 1236, "text_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a"}
    experimental_model
    Human fibroblasts from normal skin and from chronic diabetic foot ulcers
    exposure
    One hour of hyperbaric oxygen at 106 to 300 kPa, with a hydrostatic pressure control
    limitations
    A dose-response in culture with a pressure control. The authors note the effects may not be due to oxygen availability alone.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Human cells
    plain_language
    There is a best pressure, and going higher does not help more.
    primary_references
    [hbot-p16984424] Dose-dependent hyperbaric oxygen stimulation of human fibroblast proliferation. (1997). https://pubmed.ncbi.nlm.nih.gov/16984424/ DOI: 10.1046/j.1524-475x.1997.50206.x
    tissue_or_cell_type
    Dermal fibroblasts

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 803–814

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human fibroblasts from normal skin and from chronic diabetic foot ulcers · source_derived_draft · unverified_draft

    ### hbot-fibroblast-dose-response A one-hour exposure at oxygen pressures between 106 and 300 kPa increased proliferation of both normal and diabetic fibroblasts, with a dose-dependent peak at 250 kPa for normal and 200 kPa for diabetic cells, and the effects were not due to hydrostatic pressure per se. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: There is a best pressure, and going higher does not help more. organism: Human cells tissue_or_cell_type: Dermal fibroblasts experimental_model: Human fibroblasts from normal skin and from chronic diabetic foot ulcers limitations: A dose-response in culture with a pressure control. The authors note the effects may not be due to oxygen availability alone. exposure: One hour of hyperbaric oxygen at 106 to 300 kPa, with a hydrostatic pressure control evidence_span: {"source_cache": "artifacts/hbot-research/16984424.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a", "start_char": 0, "end_char": 1236, "text_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a"} [hbot-p16984424] Dose-dependent hyperbaric oxygen stimulation of human fibroblast proliferation. (1997). https://pubmed.ncbi.nlm.nih.gov/16984424/ DOI: 10.1046/j.1524-475x.1997.50206.x
    Complete structured claim and evidence

  2. Treatment promoted expression of HIF-1alpha, NF-kappaB, VEGFA, SDF-1, VEGFR2 and CXCR4, with SDF-1 and VEGFA rising in human skin fibroblasts and CXCR4 and VEGFR2 rising in endothelial cells.

    Hyperbaric oxygen therapy → Stromal cell-derived factor 1 / SDF-1alpha / CXCL12 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"}
    experimental_model
    Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells
    exposure
    Hyperbaric oxygen with high glucose in vitro
    limitations
    Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Mouse and human cells
    plain_language
    The signal and its receptor go up on two different cell types at once, which is what lets them find each other.
    primary_references
    [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246
    tissue_or_cell_type
    Skin wound, fibroblasts and endothelium

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 660–671

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells · source_derived_draft · unverified_draft

    ### hbot-hif-vegf-sdf-axis Treatment promoted expression of HIF-1alpha, NF-kappaB, VEGFA, SDF-1, VEGFR2 and CXCR4, with SDF-1 and VEGFA rising in human skin fibroblasts and CXCR4 and VEGFR2 rising in endothelial cells. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The signal and its receptor go up on two different cell types at once, which is what lets them find each other. organism: Mouse and human cells tissue_or_cell_type: Skin wound, fibroblasts and endothelium experimental_model: Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells limitations: Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person. exposure: Hyperbaric oxygen with high glucose in vitro evidence_span: {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"} [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246
    Complete structured claim and evidence

  3. Induction of fibroblast proliferation by hyperbaric oxygen disappeared when HIF-1alpha was knocked down.

    HIF-1 alpha → Human fibroblast proliferation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/hbot-research/25532619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac", "start_char": 0, "end_char": 1943, "text_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac"}
    experimental_model
    Human dermal fibroblasts, SKRC7 cells, HIF-1alpha knockout mouse embryonic fibroblasts, and db/db mice
    exposure
    Hyperbaric oxygen in vitro and in vivo, with adenoviral stable HIF-1alpha delivery
    limitations
    The knockout arm carries the causal claim. The authors describe the stabilisation as non-canonical, so the route from oxygen to HIF stability here is not the classical hydroxylase route.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Human cells and mouse
    plain_language
    Take the sensor away and the cells stop responding to the treatment.
    primary_references
    [hbot-p25532619] Hyperbaric oxygen therapy activates hypoxia-inducible factor 1 (HIF-1), which contributes to improved wound healing in diabetic mice. (2015). https://pubmed.ncbi.nlm.nih.gov/25532619/ DOI: 10.1111/wrr.12253
    tissue_or_cell_type
    Dermal fibroblasts and diabetic wounds
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 634–645

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human dermal fibroblasts, SKRC7 cells, HIF-1alpha knockout mouse embryonic fibroblasts, and db/db mice · source_derived_draft · unverified_draft

    ### hbot-hif1-required-proliferation Induction of fibroblast proliferation by hyperbaric oxygen disappeared when HIF-1alpha was knocked down. Condition category: machinery_impairment nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Take the sensor away and the cells stop responding to the treatment. organism: Human cells and mouse tissue_or_cell_type: Dermal fibroblasts and diabetic wounds experimental_model: Human dermal fibroblasts, SKRC7 cells, HIF-1alpha knockout mouse embryonic fibroblasts, and db/db mice limitations: The knockout arm carries the causal claim. The authors describe the stabilisation as non-canonical, so the route from oxygen to HIF stability here is not the classical hydroxylase route. exposure: Hyperbaric oxygen in vitro and in vivo, with adenoviral stable HIF-1alpha delivery evidence_span: {"source_cache": "artifacts/hbot-research/25532619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac", "start_char": 0, "end_char": 1943, "text_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac"} [hbot-p25532619] Hyperbaric oxygen therapy activates hypoxia-inducible factor 1 (HIF-1), which contributes to improved wound healing in diabetic mice. (2015). https://pubmed.ncbi.nlm.nih.gov/25532619/ DOI: 10.1111/wrr.12253
    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.

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