Evidence map›Paper›PMID 29069360›Full record

ArticleEndocrinology2017

Mouse Models of Primary Aldosteronism: From Physiology to Pathophysiology.

Leticia Aragao-Santiago, Celso E Gomez-Sanchez, Paolo Mulatero, Ariadni Spyroglou, Martin Reincke, Tracy Ann Williams

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. A modifiable driver of dementia: cognitive impairment in primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Review
  2. Article
  3. Alterations in glucocorticoid homeostasis following sleeve gastrectomy.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Cardiovascular diagnosis and therapy · 2023
    Article
  6. Article
  7. Article
  8. Recent advances in the developmental origin of neuroblastoma: an overview.Journal of experimental & clinical cancer research : CR · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
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

6 authors at 4 institutions in 3 countries.

Leticia Aragao-SantiagoMedizinische Klinik und Poliklinik IV, Klinikum der Ludwig-Maximilians-Universität München, Germany.
Celso E Gomez-SanchezEndocrinology Division, G.V. (Sonny) Montgomery Veterans Affairs Medical Center and University of Mississippi Medical Center.
Paolo MulateroDivision of Internal Medicine and Hypertension, Department of Medical Sciences, University of Turin, Italy.
Ariadni SpyroglouMedizinische Klinik und Poliklinik IV, Klinikum der Ludwig-Maximilians-Universität München, Germany.
Martin ReinckeMedizinische Klinik und Poliklinik IV, Klinikum der Ludwig-Maximilians-Universität München, Germany.
Tracy Ann WilliamsMedizinische Klinik und Poliklinik IV, Klinikum der Ludwig-Maximilians-Universität München, Germany.
Ludwig-Maximilians-Universität München · DELMU Klinikum · DEUniversity of Mississippi Medical Center · USUniversity of Turin · IT

Funding

Tracking and Evaluation CoreU54GM115428 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI MASON, SARAH · 2016 to 2025
$38.2M
ROLE OF MINERALOCORTICOIDS IN LOW-RENIN HYPERTENSIONR01HL027255 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI GOMEZ-SANCHEZ, CELSO ENRIQUE · 1985 to 2017
$3.9M
NHLBI NIH HHS R01 HL027255NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

Primary aldosteronism (PA) is a common form of endocrine hypertension that is characterized by the excessive production of aldosterone relative to suppressed plasma renin levels. PA is usually caused by either a unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia. Somatic mutations have been identified in several genes that encode ion pumps and channels that may explain the aldosterone excess in over half of aldosterone-producing adenomas, whereas the pathophysiology of bilateral adrenal hyperplasia is largely unknown. A number of mouse models of hyperaldosteronism have been described that recreate some features of the human disorder, although none replicate the genetic basis of human PA. Animal models that reproduce the genotype-phenotype associations of human PA are required to establish the functional mechanisms that underlie the endocrine autonomy and deregulated cell growth of the affected adrenal and for preclinical studies of novel therapeutics. Herein, we discuss the differences in adrenal physiology across species and describe the genetically modified mouse models of PA that have been developed to date.

Indexed as

Disease Models, AnimalAdenomatous Polyposis Coli ProteinAdrenal GlandsAnimalsCryptochromesHumansHyperaldosteronismLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMice, KnockoutMice, TransgenicPotassium ChannelsPotassium Channels, Tandem Pore DomainSpecies SpecificityAdenomatous Polyposis Coli ProteinCry1 protein, mouseCry2 protein, mouseCryptochromesKcnk5 protein, mouseKcnma1 protein, mouseLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsPotassium ChannelsPotassium Channels, Tandem Pore DomainTASK3 protein, mouse

Identifiers

PMID29069360
PMCPMC5711388
OpenAlexW2766387204

What OpenQuestion holds

Textmetadata
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.