Component
Human lung myofibroblast differentiation
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.
What acts on it
Combined inhibition of alanine synthesis and uptake suppressed fibrogenic responses in human fibroblasts and precision-cut lung slices.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human cells and ex vivo lung tissue; metabolic perturbations.
- limitations
- Preclinical work, not an established human antifibrotic therapy. The final paper and its preprint are one study lineage.
- nutrient_topic
- L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
- plain_language
- Blocking both supply routes had a stronger mechanistic rationale than assuming only one route mattered.
- primary_references
- TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 528–534
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cells and ex vivo lung tissue; metabolic perturbations. · source_derived_draft · unverified_draft
## alanine-fibroblast-dual-block Blocking both supply routes had a stronger mechanistic rationale than assuming only one route mattered. Combined inhibition of alanine synthesis and uptake suppressed fibrogenic responses in human fibroblasts and precision-cut lung slices. Model: Human cells and ex vivo lung tissue; metabolic perturbations. Limitations: Preclinical work, not an established human antifibrotic therapy. The final paper and its preprint are one study lineage. Evidence access: Primary full text TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449
Complete structured claim and evidenceGPT2 inhibition lowered alanine and reduced TGF-beta-induced alpha-SMA and COL1A1 expression; 2 mM exogenous alanine rescued these readouts.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human lung fibroblast perturbation and add-back experiments.
- limitations
- Marker rescue in cells is not a clinical fibrosis outcome.
- nutrient_topic
- L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
- plain_language
- Alanine add-back bypassed part of the inhibited synthesis pathway.
- primary_references
- TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 512–518
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human lung fibroblast perturbation and add-back experiments. · source_derived_draft · unverified_draft
## alanine-fibroblast-gpt2-rescue Alanine add-back bypassed part of the inhibited synthesis pathway. GPT2 inhibition lowered alanine and reduced TGF-beta-induced alpha-SMA and COL1A1 expression; 2 mM exogenous alanine rescued these readouts. Model: Human lung fibroblast perturbation and add-back experiments. Limitations: Marker rescue in cells is not a clinical fibrosis outcome. Evidence access: Primary full text TGF-β coordinates alanine synthesis and import for myofibroblast differentiation in pulmonary fibrosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42024472/ · DOI 10.1172/jci.insight.199449
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.