Angiogenesis / new blood vessel formation

evidence_span

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experimental_model

Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies

exposure

Hyperbaric oxygen with standard wound care for 20 days

limitations

A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue.

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

plain_language

Five different growth signals rose together in the treated wound.

primary_references

[hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

tissue_or_cell_type

Diabetic foot ulcer tissue

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 829–840

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies · source_derived_draft · unverified_draft

### hbot-angiogenic-markers Treatment increased tissue levels of the angiogenesis markers EGF, VEGF, PDGF, FGF-2 and CXCL10, and Nrf2 correlated positively with EGF, VEGF and PDGF. 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: Five different growth signals rose together in the treated wound. organism: Human tissue_or_cell_type: Diabetic foot ulcer tissue experimental_model: Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies limitations: A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue. exposure: Hyperbaric oxygen with standard wound care for 20 days evidence_span: {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"} [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

evidence_span

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experimental_model

Fourteen-day outcome study after middle cerebral artery occlusion in rats with BrdU labelling

exposure

Dihydrocapsaicin at 10 mg/kg body weight after 2 hours of occlusion

limitations

The dose here is roughly an order of magnitude above the hypothermia studies and no temperature is reported, so this may not be a hypothermic effect at all. Recorded with that stated.

nutrient_topic

Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin

organism

Rat

plain_language

At a much larger dose it made new blood vessels grow into the damaged area over two weeks.

primary_references

[dhc-p32107104] Dihydrocapsaicin-induced angiogenesis and improved functional recovery after cerebral ischemia and reperfusion in a rat model. (2020). https://pubmed.ncbi.nlm.nih.gov/32107104/ DOI: 10.1016/j.jphs.2020.02.001

tissue_or_cell_type

Brain vasculature

Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 465–476

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fourteen-day outcome study after middle cerebral artery occlusion in rats with BrdU labelling · source_derived_draft · unverified_draft

### dhc-angiogenesis-at-high-dose Dihydrocapsaicin at 10 mg/kg increased the expression of hypoxia inducible factor 1 alpha, vascular endothelial growth factor and matrix metalloprotease 9 at 3 and 14 days after ischaemia-reperfusion and of angiopoietin 1 and its receptor Tie-2 at 14 days, with angiogenesis confirmed by BrdU labelling co-localised with von Willebrand factor, alongside decreased neurological deficit scores and infarct volume and improved rotarod and pole test performance. 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: At a much larger dose it made new blood vessels grow into the damaged area over two weeks. organism: Rat tissue_or_cell_type: Brain vasculature experimental_model: Fourteen-day outcome study after middle cerebral artery occlusion in rats with BrdU labelling limitations: The dose here is roughly an order of magnitude above the hypothermia studies and no temperature is reported, so this may not be a hypothermic effect at all. Recorded with that stated. exposure: Dihydrocapsaicin at 10 mg/kg body weight after 2 hours of occlusion evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/32107104.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a00c09c7443e15a674b7e9c6451ddd60a161f69ff98e33c32bcce0039662f8b1", "start_char": 0, "end_char": 1350, "text_sha256": "a00c09c7443e15a674b7e9c6451ddd60a161f69ff98e33c32bcce0039662f8b1"} [dhc-p32107104] Dihydrocapsaicin-induced angiogenesis and improved functional recovery after cerebral ischemia and reperfusion in a rat model. (2020). https://pubmed.ncbi.nlm.nih.gov/32107104/ DOI: 10.1016/j.jphs.2020.02.001

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor

exposure

2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days

limitations

Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here.

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

Mopping up the reactive species, or blocking nitric oxide production, cancels the benefit.

primary_references

[hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

tissue_or_cell_type

Skeletal muscle

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 699–710

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor · source_derived_draft · unverified_draft

### hbot-nac-lname-block Administration of either N-acetylcysteine or L-NAME before treatment suppressed angiogenesis and muscle regeneration even after hyperbaric oxygen. 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: Mopping up the reactive species, or blocking nitric oxide production, cancels the benefit. organism: Rat tissue_or_cell_type: Skeletal muscle experimental_model: Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor limitations: Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here. exposure: 2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days evidence_span: {"source_cache": "artifacts/hbot-research/32066777.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d", "start_char": 0, "end_char": 1357, "text_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d"} [hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

evidence_span

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experimental_model

Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor

exposure

2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days

limitations

Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here.

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

Within a day the growth signals rise; within a week there are new vessels and repaired muscle.

primary_references

[hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

tissue_or_cell_type

Skeletal muscle

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 686–697

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor · source_derived_draft · unverified_draft

### hbot-no-vegf-bfgf Treatment significantly increased nitrate, VEGF and basic fibroblast growth factor levels and stabilised HIF-1alpha within one day, promoting blood vessel formation at 3 to 7 days and muscle healing at 5 to 7 days after contusion. 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: Within a day the growth signals rise; within a week there are new vessels and repaired muscle. organism: Rat tissue_or_cell_type: Skeletal muscle experimental_model: Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor limitations: Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here. exposure: 2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days evidence_span: {"source_cache": "artifacts/hbot-research/32066777.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d", "start_char": 0, "end_char": 1357, "text_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d"} [hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

evidence_span

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experimental_model

Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation

exposure

Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation

limitations

The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence.

nutrient_topic

Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin

organism

Rat

plain_language

It protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes.

primary_references

[dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167

tissue_or_cell_type

Skin flap vasculature

Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 699–710

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation · source_derived_draft · unverified_draft

### dhc-suppresses-sting Dihydrocapsaicin enhanced the survival of multizone perforator flaps by suppressing the cGAS-STING pathway, oxidative stress and formation of the NLRP3 inflammasome, inducing oxidative stress resistance and preventing apoptosis in vascular endothelial cells, whereas activation of the cGAS-STING pathway led to accumulation of reactive oxygen species and NLRP3 inflammasome and diminished the protective role of dihydrocapsaicin. 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 protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes. organism: Rat tissue_or_cell_type: Skin flap vasculature experimental_model: Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation limitations: The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence. exposure: Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/38459660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf", "start_char": 0, "end_char": 1793, "text_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf"} [dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167

evidence_span

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experimental_model

Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models

exposure

Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model

limitations

Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here.

nutrient_topic

Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole

organism

Mouse

plain_language

It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones.

primary_references

[mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234

tissue_or_cell_type

Medulloblastoma and tumour vasculature

Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 550–561

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models · source_derived_draft · unverified_draft

### mbz-vegfr2-atp-competition Mebendazole was determined to interfere with vascular endothelial growth factor receptor 2 kinase by competing with ATP, selectively inhibited tumour angiogenesis but not the normal brain vasculature in orthotopic medulloblastoma models, suppressed the kinase in vivo, and significantly extended survival of medulloblastoma models derived from different molecular backgrounds including a PTCH1-mutant tumour with acquired resistance to the smoothened inhibitor vismodegib. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones. organism: Mouse tissue_or_cell_type: Medulloblastoma and tumour vasculature experimental_model: Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models limitations: Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here. exposure: Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model evidence_span: {"source_cache": "artifacts/mebendazole-research/25253417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169", "start_char": 0, "end_char": 1798, "text_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169"} [mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234