Component

C-X-C chemokine receptor type 4 / CXCR4

C-X-C chemokine receptor type 4 / CXCR4. Species, exposure and limitations are retained in each linked claim.

3 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.

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. Colony-forming cells rose from 16 to 26 per 100,000 monocytes plated, entirely due to the CD34-positive subpopulation, and a high proportion of progeny cells expressed receptors for vascular endothelial growth factor-2 and for stromal-derived growth factor.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"}
    experimental_model
    Human volunteers, mice, and endothelial nitric oxide synthase knockout mice
    exposure
    2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments
    limitations
    The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel.
    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 and mouse
    plain_language
    The mobilised cells carry the receptors for the two signals that guide them to a wound.
    primary_references
    [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005
    tissue_or_cell_type
    Bone marrow and peripheral blood

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 543–554

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteers, mice, and endothelial nitric oxide synthase knockout mice · source_derived_draft · unverified_draft

    ### hbot-cfc-increase Colony-forming cells rose from 16 to 26 per 100,000 monocytes plated, entirely due to the CD34-positive subpopulation, and a high proportion of progeny cells expressed receptors for vascular endothelial growth factor-2 and for stromal-derived growth factor. 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 mobilised cells carry the receptors for the two signals that guide them to a wound. organism: Human and mouse tissue_or_cell_type: Bone marrow and peripheral blood experimental_model: Human volunteers, mice, and endothelial nitric oxide synthase knockout mice limitations: The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel. exposure: 2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments evidence_span: {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"} [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005
    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.

    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. Glutamate increased CXCR4-mediated T-cell chemotactic migration toward CXCL12 in the reported experiments.

    L-Glutamate → Human T-cell migration toward CXCL12 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human T-cell chemotaxis experiments in the receptor study.
    limitations
    This does not establish disease causation or the direction of a clinical immune effect.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    A metabolic signal interacted with a chemokine-guided movement system.
    primary_references
    Human T cells express a functional ionotropic glutamate receptor GluR3, and glutamate by itself triggers integrin-mediated adhesion to laminin and fibronectin and chemotactic migration. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12682273/ · DOI 10.4049/jimmunol.170.8.4362

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 362–368

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human T-cell chemotaxis experiments in the receptor study. · source_derived_draft · unverified_draft

    ## glutamate-immune-migration A metabolic signal interacted with a chemokine-guided movement system. Glutamate increased CXCR4-mediated T-cell chemotactic migration toward CXCL12 in the reported experiments. Model: Human T-cell chemotaxis experiments in the receptor study. Limitations: This does not establish disease causation or the direction of a clinical immune effect. Evidence access: Primary abstract Human T cells express a functional ionotropic glutamate receptor GluR3, and glutamate by itself triggers integrin-mediated adhesion to laminin and fibronectin and chemotactic migration. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12682273/ · DOI 10.4049/jimmunol.170.8.4362
    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.

    Evidence, AI assistance and curation standards