ReviewNature reviews. Endocrinology2013
Role of KCNJ5 in familial and sporadic primary aldosteronism.
Review in Nature reviews. Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Cortisol Co-Secretion and Clinical Usefulness of ACTH Stimulation Test in Primary Aldosteronism: A Systematic Review and Biases in Epidemiological Studies.Frontiers in endocrinology · 2021Pooled it
- Machine learning-based model for prediction of KCNJ5 mutation in unilateral primary aldosteronism based on [EJNMMI research · 2026Article
- Association between primary aldosteronism and type 2 diabetes and identification of potential molecular mechanisms.Frontiers in endocrinology · 2026Article
- Molecular investigation of primary aldosteronism: exploring genetic heterogeneity in understudied populations.Archives of endocrinology and metabolism · 2025Article
- An In Silico Investigation of the Pathogenic G151R G Protein-Gated Inwardly Rectifying KBiology · 2024Article
- Article
- Clinical value ofEJNMMI research · 2024Article
- Treating Primary Aldosteronism-Induced Hypertension: Novel Approaches and Future Outlooks.Endocrine reviews · 2024Article
- Evaluating the role of aldosterone synthesis on adrenal cell fate.Frontiers in endocrinology · 2024Review
- Identifying primary aldosteronism patients who require adrenal venous sampling: a multi-center study.Scientific reports · 2023Article
- Consequences of somatic mutations of GIRK1 detected in primary malign tumors on expression and function of G-protein activated, inwardly rectifying, KFrontiers in oncology · 2022Article
- False-negative aldosterone-to-renin ratio in a primary aldosteronism patient complicated with primary polydipsia: case report.Gland surgery · 2022Article
- Pathogenesis of Primary Aldosteronism: Impact on Clinical Outcome.Frontiers in endocrinology · 2022Review
- A rare case of hyporeninemic hypertension: Answers.Pediatric nephrology (Berlin, Germany) · 2021Article
- A Bibliometric Analysis of Primary Aldosteronism Research From 2000 to 2020.Frontiers in endocrinology · 2021Article
- International Histopathology Consensus for Unilateral Primary Aldosteronism.The Journal of clinical endocrinology and metabolism · 2021Article
- Pathogenesis and treatment of primary aldosteronism.Nature reviews. Endocrinology · 2020Review
- Molecular Basis of Primary Aldosteronism and Adrenal Cushing Syndrome.Journal of the Endocrine Society · 2020Review
- Genetic screening for monogenic hypertension in hypertensive individuals in a clinical setting.Journal of medical genetics · 2020Article
- Primary aldosteronism diagnostics:Gland surgery · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary aldosteronism is characterised by the dysregulation of aldosterone production and comprises both sporadic forms, caused by an aldosterone-producing adenoma or bilateral adrenal hyperplasia, and familial forms (familial hyperaldosteronism types I, II and III). The two principal physiological regulators of aldosterone synthesis are angiotensin II and serum K(+), which reverse the high resting K(+) conductance and hyperpolarized membrane potential of adrenal glomerulosa cells. The resulting membrane depolarization causes the opening of voltage-gated Ca(2+) channels and an increase in intracellular Ca(2+) that stimulates aldosterone biosynthesis. Point mutations in the KCNJ5 gene, which encodes the G-protein-activated inward rectifier K(+) channel 4 (GIRK4), have been implicated in the pathogenesis of both sporadic and familial forms of primary aldosteronism. These mutations interfere with the selectivity filter of GIRK4 causing Na(+) entry, cell depolarization and Ca(2+) channel opening, resulting in constitutive aldosterone production. Seven families with familial hyperaldosteronism caused by KCNJ5 germline mutations have so far been described, and multicentre studies have reported KCNJ5 mutations in approximately 40% of sporadic aldosterone-producing adenomas. Herein, we review the role of GIRK4 in adrenal pathophysiology and provide an overview of the clinical and biochemical phenotypes resulting from KCNJ5 mutations in patients with sporadic and familial primary aldosteronism.
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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.