Evidence map›Paper›PMID 33796077›Full record

ArticleFrontiers in endocrinology2021

Aldosterone-Regulating Receptors and Aldosterone-Driver Somatic Mutations.

Jung Soo Lim, Samuel W Plaska, Juilee Rege, William E Rainey, Adina F Turcu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Subclinical primary aldosteronism.Archives of endocrinology and metabolism · 2025
    Review
  5. Observational
  6. Article
  7. Review
  8. Adrenal Vein Sampling in Primary Aldosteronism-Is The Gold Standard Losing Its Luster?The Journal of clinical endocrinology and metabolism · 2025
    Article
  9. Article
  10. Characterizing the Origins of Primary Aldosteronism.Hypertension (Dallas, Tex. : 1979) · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Primary Aldosteronism: State-of-the-Art Review.American journal of hypertension · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Jung Soo LimDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United States.
Samuel W PlaskaDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United States.
Juilee RegeDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United States.
William E RaineyDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United States.
Adina F TurcuDivision of Metabolism, Endocrine, and Diabetes, University of Michigan, Ann Arbor, MI, United States.
University of Michigan · USWonju Severance Christian Hospital · KR

Funding

Adrenal Origins of Aldosterone ExcessR01DK106618 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI William E Rainey, Aaron Mark Udager · 2016 to 2026
$6.0M
NIDDK NIH HHS R01 DK106618
6 · The paper itself

Abstract

Background: Somatic gene mutations that facilitate inappropriate intracellular calcium entrance have been identified in most aldosterone-producing adenomas (APAs). Studies suggest that angiotensin II and adrenocorticotropic hormone (ACTH) augment aldosterone production from APAs. Little is known, however, regarding possible variations in response to hormonal stimuli between APAs with different aldosterone-driver mutations. Objective: To analyze the transcript expression of type 1 angiotensin II receptors ( Methods: RNA was isolated from APAs with mutations in: Results: Compared to adjacent normal adrenal tissue, APAs had higher transcript levels of Conclusions: While

Indexed as

MutationAdenomaAdrenal GlandsAdrenocorticotropic HormoneAdultAgedAldosteroneFemaleG Protein-Coupled Inwardly-Rectifying Potassium ChannelsHigh-Throughput Nucleotide SequencingHumansMaleMembrane ProteinsMiddle AgedReal-Time Polymerase Chain ReactionReceptor, Angiotensin, Type 1Adrenocorticotropic HormoneAGTR1 protein, humanAldosteroneCYP17A1 protein, humanG Protein-Coupled Inwardly-Rectifying Potassium ChannelsKCNJ5 protein, humanMembrane ProteinsMRAP protein, humanReceptor, Angiotensin, Type 1Receptor, Melanocortin, Type 2Receptors, CorticotropinSteroid 11-beta-HydroxylaseSteroid 17-alpha-Hydroxylaseadrenaladrenal cortexadrenocorticotropic hormone (ACTH)aldosteroneangiotensinprimary aldosteronism

Identifiers

PMID33796077
PMCPMC8008747
OpenAlexW3136762356

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.