Component
Erythropoietin
Independent biological entity. Read linked claims for experimental scope and context.
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)
Vitamin A deficiency reduced renal Epo mRNA in the rat experiment.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Renal gene-expression assay.
- limitations
- Does not by itself measure circulating EPO or prove ineffective erythropoiesis mediation.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Rattus norvegicus
- plain_language
- A shortage affected expression of an erythropoietic signal.
- primary_references
- [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
- tissue_or_cell_type
- Kidney
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1755–1764
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Renal gene-expression assay. · source_derived_draft · unverified_draft
### va-deficiency-epo-transcript Vitamin A deficiency reduced renal Epo mRNA in the rat experiment. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shortage affected expression of an erythropoietic signal. organism: Rattus norvegicus tissue_or_cell_type: Kidney experimental_model: Renal gene-expression assay. limitations: Does not by itself measure circulating EPO or prove ineffective erythropoiesis mediation. [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
Complete structured claim and evidenceVitamin A increased circulating EPO and hemoglobin in schoolchildren with poor nutrient status.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Vitamin A -> EPO/iron use.
- experimental_model
- Randomized ten-month follow-up.
- limitations
- EPO was measured, not blocked; its mediation of the hemoglobin response remains inferred.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens
- plain_language
- Vitamin A can influence the signal that supports red-cell production.
- primary_references
- [va-zimmermann2006-iron] Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron (2006). https://pubmed.ncbi.nlm.nih.gov/16960172/ DOI: 10.1093/ajcn/84.3.580
- tissue_or_cell_type
- Blood
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1460–1470
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized ten-month follow-up. · source_derived_draft · unverified_draft
### va-repletion-erythropoietin Vitamin A increased circulating EPO and hemoglobin in schoolchildren with poor nutrient status. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A can influence the signal that supports red-cell production. organism: Homo sapiens tissue_or_cell_type: Blood experimental_model: Randomized ten-month follow-up. limitations: EPO was measured, not blocked; its mediation of the hemoglobin response remains inferred. cross_nutrient: Vitamin A -> EPO/iron use. [va-zimmermann2006-iron] Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron (2006). https://pubmed.ncbi.nlm.nih.gov/16960172/ DOI: 10.1093/ajcn/84.3.580
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.