Article in Hypertension (Dallas, Tex. : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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.
Desmaré van Rooyen *Department of Molecular & Integrative Physiology (D.v.R., G.C., W.E.R., J.R.), University of Michigan, Ann Arbor, MI.ORCID 0000-0003-2969-1127
Sascha Bandulik *Medical Cell Biology, University of Regensburg, Germany (S.B., M.L., R.W.).ORCID 0000-0001-7955-7220
Grace A CoonDepartment of Molecular & Integrative Physiology (D.v.R., G.C., W.E.R., J.R.), University of Michigan, Ann Arbor, MI.ORCID 0009-0001-9114-9403
Miriam LaukemperMedical Cell Biology, University of Regensburg, Germany (S.B., M.L., R.W.).ORCID 0009-0004-6151-1573
Chandan Kumar-SinhaRogel Cancer Center (C.K.-S., A.M.U.), University of Michigan, Ann Arbor, MI.ORCID 0000-0002-8696-3400
Aaron M UdagerRogel Cancer Center (C.K.-S., A.M.U.), University of Michigan, Ann Arbor, MI.ORCID 0000-0002-8254-5404
Antonio M LerarioDivision of Metabolism, Endocrine, and Diabetes, Department of Internal Medicine (D.v.R, A.M.L., C.L., A.F.T., W.E.R.), University of Michigan, Ann Arbor, MI.ORCID 0000-0002-8336-6432
Chaelin LeeDivision of Metabolism, Endocrine, and Diabetes, Department of Internal Medicine (D.v.R, A.M.L., C.L., A.F.T., W.E.R.), University of Michigan, Ann Arbor, MI.ORCID 0000-0002-0490-2437
Heather WachtelDepartment of Surgery (H.W.), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.ORCID 0000-0003-3786-3638
Debbie L CohenDepartment of Medicine, Renal, Electrolyte and Hypertension Division (D.L.C.), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.ORCID 0000-0002-1325-315X
James M LutherDepartment of Medicine, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN (J.M.L.).ORCID 0000-0001-7225-2897
Thomas J GiordanoDepartment of Pathology (A.M.U., T.G.), University of Michigan, Ann Arbor, MI.ORCID 0000-0003-0641-8873
Ute I SchollCenter of Functional Genomics, Berlin Institute of Health at Charité-Universitätsmedizin Berlin, Berlin, Germany (U.I.S, B.P.).ORCID 0000-0002-0309-8045
Frederike ButzDepartment of Surgery, Campus Charité Mitte | Campus Virchow-Klinikum, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany (F.B.).ORCID 0000-0002-5963-1558
Bernt PoppCenter of Functional Genomics, Berlin Institute of Health at Charité-Universitätsmedizin Berlin, Berlin, Germany (U.I.S, B.P.).ORCID 0000-0002-3679-1081
Adina F TurcuDivision of Metabolism, Endocrine, and Diabetes, Department of Internal Medicine (D.v.R, A.M.L., C.L., A.F.T., W.E.R.), University of Michigan, Ann Arbor, MI.ORCID 0000-0001-9831-6190
Richard WarthMedical Cell Biology, University of Regensburg, Germany (S.B., M.L., R.W.).ORCID 0000-0001-6084-0659
William E RaineyDepartment of Molecular & Integrative Physiology (D.v.R., G.C., W.E.R., J.R.), University of Michigan, Ann Arbor, MI.ORCID 0000-0001-5557-8406
Juilee RegeDepartment of Molecular & Integrative Physiology (D.v.R., G.C., W.E.R., J.R.), University of Michigan, Ann Arbor, MI.ORCID 0000-0003-2593-5008
Funding
Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ben Ho Park · 1995 to 2026
$172.8M
Vanderbilt Institute for Clinical and Translational Research (VICTR) -Identifying correlates of functional immunity in SARS-CoV-2 convalescent plasmaUL1TR002243 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Paul A. Harris, Wesley H Self · 2017 to 2026
$130.7M
Michigan Institute for Clinical and Health Research (MICHR)UL1TR002240 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUMENG, JULIE C, MASHOUR, GEORGE ALEXANDER · 2017 to 2022
$54.9M
Adrenal Origins of Aldosterone ExcessR01DK106618 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI William E Rainey, Aaron Mark Udager · 2016 to 2026
$6.0M
Primary Aldosteronism Subtypes: Pathophysiology and Steroid SignaturesR01HL155834 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TURCU, ADINA F · 2021 to 2025
$3.5M
11-Oxyandrogens and Aging: Health ImplicationsR01AG080516 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Adina F Turcu · 2023 to 2026
$2.3M
Endogenous Aldosterone and Glucose HomeostasisR01DK096994 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LUTHER, JAMES MATTHEW · 2013 to 2017
$2.1M
Genetic Causes of Endocrine Hypertension in Black AmericansR01HL174676 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Juilee Rege · 2024 to 2026
$1.1M
A genotype-phenotype study of germline succinate dehydrogenase pathogenic variantsK08CA270385 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Heather Wachtel · 2022 to 2026
backgroundPrimary aldosteronism is a common but underdiagnosed cause of endocrine hypertension that contributes to global cardiovascular morbidity and mortality. It is characterized by renin-independent hyperaldosteronism that originates from adrenal lesions-the majority of which are found to harbor aldosterone-driver somatic mutations in genes encoding ion-transporting proteins. These mutations disrupt intracellular calcium homeostasis, facilitating a pathological increase in aldosterone synthase expression and aldosterone production. Elucidating the exact mechanisms causing aldosterone excess in primary aldosteronism would further the development of targeted treatments and alleviate the global hypertension burden.
methodsNext-generation sequencing analysis of formalin-fixed paraffin-embedded aldosterone-producing adenomas identified novel somatic variants in
resultsThree somatic
conclusionsThis is the first report of disease-causing
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 Socratic graph.