Component

RhoA

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

2 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

What acts on it

  1. Ibuprofen activates peroxisome proliferator-activated receptor gamma in neuron-like PC12 and B104 cells, activation with traditional agonists mimics the RhoA-inhibiting properties of ibuprofen and promotes neurite elongation in primary neurons exposed to axonal growth inhibitors, small interfering RNA against the receptor blocks RhoA suppression by those agonists, and selective receptor inhibition prevents the effect of ibuprofen on RhoA activity and neurite growth, supporting an essential role for the receptor in coupling ibuprofen to RhoA inhibition.

    Human PPAR gamma / PPARG → RhoA source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/20089905.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3", "start_char": 0, "end_char": 1812, "text_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3"}
    experimental_model
    Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown
    exposure
    Ibuprofen with peroxisome proliferator-activated receptor gamma agonists, antagonists and knockdown
    limitations
    The knockdown and the selective antagonist together make the receptor requirement a test rather than a correlation. Cell lines and primary culture rather than an animal.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Rat
    plain_language
    The drug reaches a growth-blocking switch in neurons through a fat-sensing receptor, not through prostaglandins.
    primary_references
    [ibu-p20089905] A molecular mechanism for ibuprofen-mediated RhoA inhibition in neurons. (2010). https://pubmed.ncbi.nlm.nih.gov/20089905/ DOI: 10.1523/jneurosci.5045-09.2010
    tissue_or_cell_type
    Neurons

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 422–433

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown · source_derived_draft · unverified_draft

    ### ibu-pparg-couples-to-rhoa Ibuprofen activates peroxisome proliferator-activated receptor gamma in neuron-like PC12 and B104 cells, activation with traditional agonists mimics the RhoA-inhibiting properties of ibuprofen and promotes neurite elongation in primary neurons exposed to axonal growth inhibitors, small interfering RNA against the receptor blocks RhoA suppression by those agonists, and selective receptor inhibition prevents the effect of ibuprofen on RhoA activity and neurite growth, supporting an essential role for the receptor in coupling ibuprofen to RhoA inhibition. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The drug reaches a growth-blocking switch in neurons through a fat-sensing receptor, not through prostaglandins. organism: Rat tissue_or_cell_type: Neurons experimental_model: Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown limitations: The knockdown and the selective antagonist together make the receptor requirement a test rather than a correlation. Cell lines and primary culture rather than an animal. exposure: Ibuprofen with peroxisome proliferator-activated receptor gamma agonists, antagonists and knockdown evidence_span: {"source_cache": "artifacts/ibuprofen-research/20089905.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3", "start_char": 0, "end_char": 1812, "text_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3"} [ibu-p20089905] A molecular mechanism for ibuprofen-mediated RhoA inhibition in neurons. (2010). https://pubmed.ncbi.nlm.nih.gov/20089905/ DOI: 10.1523/jneurosci.5045-09.2010
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Chronic hypoxia decreased RhoA messenger RNA and protein expression in rat main pulmonary artery and abolished RhoA-mediated calcium sensitisation of contraction, accounting for the decreased responses to endothelin-1, noradrenaline and a thromboxane analogue, and treatment with sildenafil at 25 milligrams per kilogram daily throughout the exposure prevented the downregulation of RhoA, the reduction of contraction and the pulmonary artery remodelling, indicating a major role of the nitric oxide and cyclic GMP pathway in the altered RhoA signalling.

    Sildenafil → RhoA and Rho-kinase-mediated calcium sensitisation of contraction source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sildenafil-research/12946946.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7", "start_char": 0, "end_char": 1768, "text_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7"}
    experimental_model
    Rat pulmonary artery contractility and RhoA expression after two weeks of chronic hypoxia
    exposure
    Sildenafil 25 milligrams per kilogram daily through two weeks of 10 percent oxygen, with real-time PCR and western blotting
    limitations
    Identifies a second arm of the mechanism beyond cyclic-GMP-mediated relaxation. A rat chronic hypoxia model, and the causal chain from cyclic GMP to RhoA expression is inferred rather than dissected.
    nutrient_topic
    Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. · Sildenafil
    organism
    Rat
    plain_language
    Beyond relaxing the vessel, the drug preserved the contractile machinery that chronic low oxygen otherwise degrades.
    primary_references
    [sil-p12946946] Sildenafil prevents change in RhoA expression induced by chronic hypoxia in rat pulmonary artery. (2003). https://pubmed.ncbi.nlm.nih.gov/12946946/ DOI: 10.1161/01.res.0000093220.90027.d9
    tissue_or_cell_type
    Pulmonary artery

    Sildenafil: the enzyme it occupies instead of the substrate, why it cannot start a signal it can only preserve, the organic nitrate interaction that follows from that, the homologous retinal enzyme ten-fold away, and the pulmonary circulation where the same mechanism became a second indication (2026-09-22) · lines 548–559

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pulmonary artery contractility and RhoA expression after two weeks of chronic hypoxia · source_derived_draft · unverified_draft

    ### sil-prevents-rhoa-downregulation Chronic hypoxia decreased RhoA messenger RNA and protein expression in rat main pulmonary artery and abolished RhoA-mediated calcium sensitisation of contraction, accounting for the decreased responses to endothelin-1, noradrenaline and a thromboxane analogue, and treatment with sildenafil at 25 milligrams per kilogram daily throughout the exposure prevented the downregulation of RhoA, the reduction of contraction and the pulmonary artery remodelling, indicating a major role of the nitric oxide and cyclic GMP pathway in the altered RhoA signalling. Condition category: normal nutrient_topic: Sildenafil research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from its N-desmethyl metabolite and its target enzyme from the homologous retinal PDE6. plain_language: Beyond relaxing the vessel, the drug preserved the contractile machinery that chronic low oxygen otherwise degrades. organism: Rat tissue_or_cell_type: Pulmonary artery experimental_model: Rat pulmonary artery contractility and RhoA expression after two weeks of chronic hypoxia limitations: Identifies a second arm of the mechanism beyond cyclic-GMP-mediated relaxation. A rat chronic hypoxia model, and the causal chain from cyclic GMP to RhoA expression is inferred rather than dissected. exposure: Sildenafil 25 milligrams per kilogram daily through two weeks of 10 percent oxygen, with real-time PCR and western blotting evidence_span: {"source_cache": "artifacts/sildenafil-research/12946946.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7", "start_char": 0, "end_char": 1768, "text_sha256": "ce3f4a451c01082a280ebffc7e9661ec5667161f4974b39ba15c52fa940754f7"} [sil-p12946946] Sildenafil prevents change in RhoA expression induced by chronic hypoxia in rat pulmonary artery. (2003). https://pubmed.ncbi.nlm.nih.gov/12946946/ DOI: 10.1161/01.res.0000093220.90027.d9
    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