ReviewMolecular and cellular endocrinology2015
Somatic mutations of the ATP1A1 gene and aldosterone-producing adenomas.
Review in Molecular and cellular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Prevalence and clinical correlates of somatic mutation in aldosterone producing adenoma-Taiwanese population.Scientific reports · 2015Trial
- pH-Controlled Chemoselective Rapid Azo-Coupling Reaction (CRACR) Enables Global Profiling of Serotonylation Proteome in Cancer Cells.Journal of proteome research · 2024Article
- Diseases caused by mutations in the NaAmerican journal of physiology. Cell physiology · 2021Review
- On the effect of hyperaldosteronism-inducing mutations in Na/K pumps.The Journal of general physiology · 2017Article
- ARMC5 mutation analysis in patients with primary aldosteronism and bilateral adrenal lesions.Journal of human hypertension · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Primary aldosteronism is the most common form of secondary hypertension. It affects approximately 10% of patients with hypertension and causes greater cardiovascular morbidity and mortality compared to essential hypertension of similar severity and duration. The cause of primary aldosteronism in about half of these patients is an aldosterone-producing adenoma; over half of these adenomas have mutations in one of several ion channels and pumps, including the potassium channel KCNJ5, calcium channel Cav1.3, α1 subunit of the sodium potassium ATPase, and membrane calcium ATPase 3. This review concentrates on the molecular and physiological mechanisms by which mutations of the ATP1A1 gene increase aldosterone production.
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Registered trials
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.