Component

Human SERPINE1 / plasminogen activator inhibitor 1

Human SERPINE1 / plasminogen activator inhibitor 1. Species, exposure and limitations are retained in each linked claim.

3 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. Subtilisin NAT cleaved active recombinant PAI-1 at its reactive-site Arg346-Met347 bond and PAI-1 lost specific activity dose-dependently over 0.02-1.0 nM, with a half-maximal effect near 0.1 nM.

    Nattokinase / subtilisin NAT → Human SERPINE1 / plasminogen activator inhibitor 1 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Recombinant human PAI-1
    exposure
    Subtilisin NAT, 0.02-1.0 nM
    limitations
    The substrate was active recombinant prokaryotic PAI-1. Whether latent or vitronectin-bound PAI-1 is cleaved was not established by this work or by anything else read here.
    organism
    Recombinant human PAI-1
    plain_language
    Subtilisin NAT cleaved active recombinant PAI-1 at its reactive-site Arg346-Met347 bond and PAI-1 lost specific activity dose-dependently over 0.02-1.0 nM, with a half-maximal effect near 0.1 nM.
    primary_references
    The profibrinolytic enzyme subtilisin NAT purified from Bacillus subtilis Cleaves and inactivates plasminogen activator inhibitor type 1. (2001) https://pubmed.ncbi.nlm.nih.gov/11325965/ DOI: 10.1074/jbc.M101751200
    route
    In vitro
    tissue
    Purified-protein proteolysis with MALDI-TOF and peptide sequencing

    Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 136–136

    Original AI-assisted curation built from a supplied entity-first document of 105 entities and 129 claims. Every reference in that document was resolved against live PubMed with its abstract read and its DOI cross-checked on 2026-09-23, and the EFSA novel-food opinion was retrieved and read in full. That check corrected two PMIDs that pointed at unrelated papers, two DOIs, and two papers recorded as carrying no erratum that do carry one; it also reversed three findings the supplied document had stated backwards. Two papers carry a published correction, recorded as such and not as a retraction. Three sources are not indexed in PubMed and are cited by what they have. Laboratory lineages are recorded, so the four papers from one group, the three from another and the two readings of a single applicant dossier cannot be counted as separate lines of support. Study-specific doses, units, populations and limitations retained; activity units are never converted between systems. Not publisher full text. · supports · Recombinant human PAI-1 · source_derived_draft · unverified_draft

    Subtilisin NAT cleaved active recombinant PAI-1 at its reactive-site Arg346-Met347 bond and PAI-1 lost specific activity dose-dependently over 0.02-1.0 nM, with a half-maximal effect near 0.1 nM.
    Complete structured claim and evidence

  2. In the same cells, nattokinase reduced adrenaline-stimulated secretion of plasminogen activator inhibitor 1.

    Nattokinase / subtilisin NAT → Human SERPINE1 / plasminogen activator inhibitor 1 source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human umbilical vein endothelial cells
    exposure
    Nattokinase
    limitations
    A second route to lower PAI-1 that is not proteolysis of the inhibitor. Whether it needs catalytic activity was not tested.
    organism
    Human umbilical vein endothelial cells
    plain_language
    In the same cells, nattokinase reduced adrenaline-stimulated secretion of plasminogen activator inhibitor 1.
    primary_references
    Mechanisms of Nattokinase in protection of cerebral ischemia. (2014) https://pubmed.ncbi.nlm.nih.gov/25446567/ DOI: 10.1016/j.ejphar.2014.10.024
    route
    In vitro
    tissue
    Cultured endothelium, adrenaline-stimulated

    Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 455–455

    Original AI-assisted curation built from a supplied entity-first document of 105 entities and 129 claims. Every reference in that document was resolved against live PubMed with its abstract read and its DOI cross-checked on 2026-09-23, and the EFSA novel-food opinion was retrieved and read in full. That check corrected two PMIDs that pointed at unrelated papers, two DOIs, and two papers recorded as carrying no erratum that do carry one; it also reversed three findings the supplied document had stated backwards. Two papers carry a published correction, recorded as such and not as a retraction. Three sources are not indexed in PubMed and are cited by what they have. Laboratory lineages are recorded, so the four papers from one group, the three from another and the two readings of a single applicant dossier cannot be counted as separate lines of support. Study-specific doses, units, populations and limitations retained; activity units are never converted between systems. Not publisher full text. · supports · Human umbilical vein endothelial cells · source_derived_draft · unverified_draft

    In the same cells, nattokinase reduced adrenaline-stimulated secretion of plasminogen activator inhibitor 1.
    Complete structured claim and evidence

  3. The bark oil reduced PAI-1 production in the stimulated human dermal-fibroblast system.

    Commercial C. zeylanicum bark oil in the 2017 fibroblast study → Human SERPINE1 / plasminogen activator inhibitor 1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ceylon-research/28444928.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53", "start_char": 0, "end_char": 1601, "text_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53"}
    experimental_model
    Stimulated primary human dermal-fibroblast biomarker screen
    exposure
    Commercial C. zeylanicum bark oil in cell culture
    limitations
    Antiproliferative activity accompanies biomarker changes; reduced signal is not demonstrated safe wound healing or benefit from ingestion/topical use.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Human
    plain_language
    This was a change in a cultured-cell inflammation model, not a demonstrated clinical skin benefit.
    primary_references
    [ceylon-p28444928] Antiinflammatory Activity of Cinnamon (Cinnamomum zeylanicum) Bark Essential Oil in a Human Skin Disease Model. (2017). https://pubmed.ncbi.nlm.nih.gov/28444928/ DOI: 10.1002/ptr.5822
    tissue_or_cell_type
    Dermal fibroblast inflammatory/fibrotic model

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 1065–1076

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stimulated primary human dermal-fibroblast biomarker screen · source_derived_draft · unverified_draft

    ### ceylon-pai1 The bark oil reduced PAI-1 production in the stimulated human dermal-fibroblast system. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: This was a change in a cultured-cell inflammation model, not a demonstrated clinical skin benefit. organism: Human tissue_or_cell_type: Dermal fibroblast inflammatory/fibrotic model experimental_model: Stimulated primary human dermal-fibroblast biomarker screen limitations: Antiproliferative activity accompanies biomarker changes; reduced signal is not demonstrated safe wound healing or benefit from ingestion/topical use. exposure: Commercial C. zeylanicum bark oil in cell culture evidence_span: {"source_cache": "artifacts/ceylon-research/28444928.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53", "start_char": 0, "end_char": 1601, "text_sha256": "8abd44e4f6be7090f7789d8a303e7e7ad9b0070bc22ad6c22354fdfd1fbbfb53"} [ceylon-p28444928] Antiinflammatory Activity of Cinnamon (Cinnamomum zeylanicum) Bark Essential Oil in a Human Skin Disease Model. (2017). https://pubmed.ncbi.nlm.nih.gov/28444928/ DOI: 10.1002/ptr.5822
    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