Component
Muscle atrophy
Muscle atrophy. Species, exposure and limitations are retained in each linked claim.
1 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
DIM attenuated dexamethasone-induced myotube and mouse muscle atrophy and improved mouse grip-strength measures.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dim-research/42308990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb", "start_char": 0, "end_char": 2803, "text_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb"}
- experimental_model
- Dexamethasone atrophy and aging-model experiments
- exposure
- DIM in experimental atrophy/aging models
- limitations
- 2026 preclinical study, not a human sarcopenia trial. Mouse STIM1 stays distinct from the human selenium-linked STIM1 record.
- nutrient_topic
- Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
- organism
- Mouse muscle, mouse C2C12 myotubes and C. elegans
- plain_language
- This is a candidate mechanism to test in humans, not an established treatment.
- primary_references
- [dim-p42308990] 3,3'-Diindolylmethane ameliorates muscle atrophy by modulating mitochondrial function and calcium homeostasis. (2026). https://pubmed.ncbi.nlm.nih.gov/42308990/ DOI: 10.1016/j.phymed.2026.158409
- tissue_or_cell_type
- Mitochondrial function and store-operated calcium entry
Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1481–1492
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dexamethasone atrophy and aging-model experiments · source_derived_draft · unverified_draft
### dim-muscle-atrophy DIM attenuated dexamethasone-induced myotube and mouse muscle atrophy and improved mouse grip-strength measures. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: This is a candidate mechanism to test in humans, not an established treatment. organism: Mouse muscle, mouse C2C12 myotubes and C. elegans tissue_or_cell_type: Mitochondrial function and store-operated calcium entry experimental_model: Dexamethasone atrophy and aging-model experiments limitations: 2026 preclinical study, not a human sarcopenia trial. Mouse STIM1 stays distinct from the human selenium-linked STIM1 record. exposure: DIM in experimental atrophy/aging models evidence_span: {"source_cache": "artifacts/dim-research/42308990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb", "start_char": 0, "end_char": 2803, "text_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb"} [dim-p42308990] 3,3'-Diindolylmethane ameliorates muscle atrophy by modulating mitochondrial function and calcium homeostasis. (2026). https://pubmed.ncbi.nlm.nih.gov/42308990/ DOI: 10.1016/j.phymed.2026.158409
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.