Component
Heat shock protein 90
Heat shock protein 90. Species, exposure and limitations are retained in each linked claim.
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.
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.
Where it participates (unsigned role)
Heat shock protein 32 expression increased significantly and peaked 12 hours after exposure, while heat shock proteins 27, 70 and 90 showed only slight and non-significant increases.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/hbot-research/24465817.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f", "start_char": 0, "end_char": 1501, "text_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f"}
- experimental_model
- Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors
- exposure
- A single hyperbaric oxygen exposure before hydrogen peroxide or oxygen-glucose deprivation
- limitations
- A preconditioning experiment in cultured neurons. Heat shock protein 32 is heme oxygenase-1 under another name, which is why the inhibitor used is a porphyrin.
- 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
- Rat
- plain_language
- One heat shock protein responded strongly and the others barely moved.
- primary_references
- [hbot-p24465817] Hyperbaric oxygen preconditioning induces tolerance against oxidative injury and oxygen-glucose deprivation by up-regulating heat shock protein 32 in rat spinal neurons. (2014). https://pubmed.ncbi.nlm.nih.gov/24465817/ DOI: 10.1371/journal.pone.0085967
- tissue_or_cell_type
- Primary spinal neurons
Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 348–359
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors · source_derived_draft · unverified_draft
### hbot-hsp32-induction Heat shock protein 32 expression increased significantly and peaked 12 hours after exposure, while heat shock proteins 27, 70 and 90 showed only slight and non-significant increases. 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: One heat shock protein responded strongly and the others barely moved. organism: Rat tissue_or_cell_type: Primary spinal neurons experimental_model: Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors limitations: A preconditioning experiment in cultured neurons. Heat shock protein 32 is heme oxygenase-1 under another name, which is why the inhibitor used is a porphyrin. exposure: A single hyperbaric oxygen exposure before hydrogen peroxide or oxygen-glucose deprivation evidence_span: {"source_cache": "artifacts/hbot-research/24465817.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f", "start_char": 0, "end_char": 1501, "text_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f"} [hbot-p24465817] Hyperbaric oxygen preconditioning induces tolerance against oxidative injury and oxygen-glucose deprivation by up-regulating heat shock protein 32 in rat spinal neurons. (2014). https://pubmed.ncbi.nlm.nih.gov/24465817/ DOI: 10.1371/journal.pone.0085967
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.