Evidence map›Paper›PMID 31884735›Full record

ReviewEndocrinology and metabolism (Seoul, Korea)2019

Molecular Mechanisms of Primary Aldosteronism.

Sergei G Tevosian, Shawna C Fox, Hans K Ghayee

Open access · diamondAbstract readReview
In one paragraph

Review in Endocrinology and metabolism (Seoul, Korea), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Subunit-Specific Developmental Roles of PI3K in SF1-Expressing Cells.Endocrinology and metabolism (Seoul, Korea) · 2024
    Article
  3. Article
  4. Review
  5. Review
  6. Diseases caused by mutations in the NaAmerican journal of physiology. Cell physiology · 2021
    Review
  7. 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

3 authors at 2 institutions in 1 country.

Sergei G TevosianDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA.ORCID 0000-0001-7281-5792
Shawna C FoxDepartment of Pharmacotherapy and Translational Research, College of Pharmacy, University of Florida, Gainesville, FL, USA.
Hans K GhayeeDivision of Endocrinology, Department of Medicine, Malcom Randall VA Medical Center, University of Florida, Gainesville, FL, USA. hans.ghayee@medicine.ufl.edu.ORCID 0000-0001-9201-3033
University of Florida · USMalcom Randall VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary aldosteronism (PA) results from excess production of mineralocorticoid hormone aldosterone by the adrenal cortex. It is normally caused either by unilateral aldosterone-producing adenoma (APA) or by bilateral aldosterone excess as a result of bilateral adrenal hyperplasia. PA is the most common cause of secondary hypertension and associated morbidity and mortality. While most cases of PA are sporadic, an important insight into this debilitating disease has been derived through investigating the familial forms of the disease that affect only a minor fraction of PA patients. The advent of gene expression profiling has shed light on the genes and intracellular signaling pathways that may play a role in the pathogenesis of these tumors. The genetic basis for several forms of familial PA has been uncovered in recent years although the list is likely to expand. Recently, the work from several laboratories provided evidence for the involvement of mammalian target of rapamycin pathway and inflammatory cytokines in APAs; however, their mechanism of action in tumor development and pathophysiology remains to be understood.

Indexed as

AldosteroneAnimalsHumansHyperaldosteronismInflammation MediatorsTOR Serine-Threonine KinasesAldosteroneInflammation MediatorsTOR Serine-Threonine KinasesHyperaldosteronismHypertensionMineralocorticoids

Identifiers

PMID31884735
PMCPMC6935778
OpenAlexW2997250550

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.