Component
Human fibroblast proliferation
Human fibroblast proliferation. Species, exposure and limitations are retained in each linked claim.
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
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.
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 evidenceInduction of fibroblast proliferation by hyperbaric oxygen disappeared when HIF-1alpha was knocked down.
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
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.