Component
Human von Willebrand factor / VWF
The multimeric adhesive plasma glycoprotein whose ultralarge forms promote arterial thrombosis. The A2 domain holds the scissile bonds recorded in this chapter.
2 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.
What acts on it
Nattokinase directly cleaved the folded von Willebrand factor A2 domain and the unstructured vWF73 peptide under static conditions, with Thr1608-Gly1609 as the primary site.
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
- Purified human von Willebrand factor constructs
- exposure
- Purified nattokinase
- limitations
- A purified-substrate system. The cleaved bond sits three residues downstream of the ADAMTS13 site Tyr1605-Met1606. No multimer endpoint and no human oral exposure were measured.
- organism
- Purified human von Willebrand factor constructs
- plain_language
- Nattokinase directly cleaved the folded von Willebrand factor A2 domain and the unstructured vWF73 peptide under static conditions, with Thr1608-Gly1609 as the primary site.
- primary_references
- Degradation mechanism of the von Willebrand factor A2 domain by nattokinase. (2026) https://pubmed.ncbi.nlm.nih.gov/42163571/ DOI: 10.1002/1873-3468.70366
- route
- In vitro
- tissue
- In vitro enzymology with mass spectrometry
Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 169–169
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 · Purified human von Willebrand factor constructs · source_derived_draft · unverified_draft
Nattokinase directly cleaved the folded von Willebrand factor A2 domain and the unstructured vWF73 peptide under static conditions, with Thr1608-Gly1609 as the primary site.
Complete structured claim and evidenceA decrease in von Willebrand factor was seen in the female participants taking nattokinase, at p < 0.1.
Experimental context and source evidence
- duration
- 8 weeks
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Human (74 completers with elevated blood pressure)
- exposure
- NSK-SD, 100 mg per day
- limitations
- Exploratory, sex-restricted and above the conventional significance threshold. It is the only human measurement in this chapter that touches the von Willebrand factor mechanism, which makes it worth recording and makes over-reading it easy.
- organism
- Human (74 completers with elevated blood pressure)
- plain_language
- A decrease in von Willebrand factor was seen in the female participants taking nattokinase, at p < 0.1.
- primary_references
- Consumption of nattokinase is associated with reduced blood pressure and von Willebrand factor, a cardiovascular risk marker: results from a randomized, double-blind, placebo-controlled, multicenter North American clinical trial. (2016) https://pubmed.ncbi.nlm.nih.gov/27785095/ DOI: 10.2147/IBPC.S99553
- route
- In vivo, oral
- tissue
- Plasma
Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 1027–1027
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 (74 completers with elevated blood pressure) · source_derived_draft · unverified_draft
A decrease in von Willebrand factor was seen in the female participants taking nattokinase, at p < 0.1.
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.