Component
Plasma membrane rupture in human macrophages
Context-specific entity; species, compartment and exposure are stated on each claim.
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.
Where it participates (unsigned role)
In primary human macrophages, 50 mM glycine inhibited pyroptosis-associated NINJ1 clustering and membrane rupture; NINJ1 knockdown produced a similar rupture phenotype.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human monocyte-derived macrophages, LPS/nigericin, native-protein analysis and knockdown.
- limitations
- Direct or indirect target engagement remains unresolved; 50 mM bath exposure is not a dietary plasma concentration.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- The membrane effect also occurred in human cells at a much higher experimental exposure.
- primary_references
- Glycine inhibits NINJ1 membrane clustering to suppress plasma membrane rupture in cell death. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36468682/ · DOI 10.7554/eLife.78609
Glycine: supply, one-carbon allocation, receptors 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 monocyte-derived macrophages, LPS/nigericin, native-protein analysis and knockdown. · source_derived_draft · unverified_draft
## glycine-ninj1-human-clustering The membrane effect also occurred in human cells at a much higher experimental exposure. In primary human macrophages, 50 mM glycine inhibited pyroptosis-associated NINJ1 clustering and membrane rupture; NINJ1 knockdown produced a similar rupture phenotype. Model: Human monocyte-derived macrophages, LPS/nigericin, native-protein analysis and knockdown. Limitations: Direct or indirect target engagement remains unresolved; 50 mM bath exposure is not a dietary plasma concentration. Evidence access: Primary full text Glycine inhibits NINJ1 membrane clustering to suppress plasma membrane rupture in cell death. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36468682/ · DOI 10.7554/eLife.78609
Complete structured claim and evidenceHuman pyroptotic macrophages protected from rupture by glycine still lost mitochondrial membrane potential and ATP.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Primary human macrophage energy/viability measurements alongside LDH assays.
- limitations
- The outcome is suppression of rupture, not reversal of upstream cell death.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- An intact membrane did not mean the cell survived.
- primary_references
- Glycine inhibits NINJ1 membrane clustering to suppress plasma membrane rupture in cell death. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36468682/ · DOI 10.7554/eLife.78609
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 370–376
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary human macrophage energy/viability measurements alongside LDH assays. · source_derived_draft · unverified_draft
## glycine-ninj1-viability-limit An intact membrane did not mean the cell survived. Human pyroptotic macrophages protected from rupture by glycine still lost mitochondrial membrane potential and ATP. Model: Primary human macrophage energy/viability measurements alongside LDH assays. Limitations: The outcome is suppression of rupture, not reversal of upstream cell death. Evidence access: Primary full text Glycine inhibits NINJ1 membrane clustering to suppress plasma membrane rupture in cell death. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36468682/ · DOI 10.7554/eLife.78609
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.