Component
Mouse aquaporin 2 / Aqp2
Mouse aquaporin 2 / Aqp2. Species, exposure and limitations are retained in each linked claim.
3 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
Mangiferin reduced renal AQP2 protein expression in nephropathy mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"}
- experimental_model
- Mouse hyperuricemic nephropathy experiment
- exposure
- Mangiferin in the study-specific nephropathy model
- limitations
- Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity.
- nutrient_topic
- Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
- organism
- Mus musculus
- plain_language
- Water-handling machinery changed in this model.
- primary_references
- [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
- tissue_or_cell_type
- Kidney and metabolic-cage urine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1017–1028
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hyperuricemic nephropathy experiment · source_derived_draft · unverified_draft
### mangiferin-aqp2 Mangiferin reduced renal AQP2 protein expression in nephropathy mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Water-handling machinery changed in this model. organism: Mus musculus tissue_or_cell_type: Kidney and metabolic-cage urine experimental_model: Mouse hyperuricemic nephropathy experiment limitations: Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity. exposure: Mangiferin in the study-specific nephropathy model evidence_span: {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"} [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
Complete structured claim and evidenceChronic lithium reduced AQP2 in cortex/outer medulla and inner medulla of control mice.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse collecting-duct study.
- limitations
- Residual inner-medullary reduction persisted in Scnn1a knockout; not every AQP2 change required this entry route.
- nutrient_topic
- Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
- plain_language
- Fewer water channels can reduce water recovery from urine.
- primary_references
- alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21051735/ · DOI 10.1681/ASN.2010070734
Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 328–334
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse collecting-duct study. · source_derived_draft · unverified_draft
## lithium-aqp2-down Fewer water channels can reduce water recovery from urine. Chronic lithium reduced AQP2 in cortex/outer medulla and inner medulla of control mice. Model: Mouse collecting-duct study. Limitations: Residual inner-medullary reduction persisted in Scnn1a knockout; not every AQP2 change required this entry route. Evidence access: Primary abstract alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21051735/ · DOI 10.1681/ASN.2010070734
Complete structured claim and evidence
Where it participates (unsigned role)
Collecting-duct Scnn1a deletion protected lithium-treated mice against polyuria and loss of urine concentration.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Collecting-duct-specific mouse knockout and chronic lithium treatment.
- limitations
- Protection supports ENaC-mediated entry; connecting-tubule expression remained intact.
- nutrient_topic
- Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
- plain_language
- A sodium channel helps lithium reach vulnerable kidney cells.
- primary_references
- alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21051735/ · DOI 10.1681/ASN.2010070734
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 320–326
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Collecting-duct-specific mouse knockout and chronic lithium treatment. · source_derived_draft · unverified_draft
## lithium-enac-entry A sodium channel helps lithium reach vulnerable kidney cells. Collecting-duct Scnn1a deletion protected lithium-treated mice against polyuria and loss of urine concentration. Model: Collecting-duct-specific mouse knockout and chronic lithium treatment. Limitations: Protection supports ENaC-mediated entry; connecting-tubule expression remained intact. Evidence access: Primary abstract alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21051735/ · DOI 10.1681/ASN.2010070734
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.