Evidence map›Paper›PMID 39484451›Full record

ArticlebioRxiv : the preprint server for biology2024

Somatic Mutations in

Desmaré van Rooyen, Sascha Bandulik, Grace Coon, Miriam Laukemper, Chandan Kumar-Sinha, Aaron M Udager, Chaelin Lee, Heather Wachtel, Debbie L Cohen, James M Luther and 5 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Funding

Adrenal Origins of Aldosterone ExcessR01DK106618 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI William E Rainey, Aaron Mark Udager · 2016 to 2026
$6.0M
Genetic Causes of Endocrine Hypertension in Black AmericansR01HL174676 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Juilee Rege · 2024 to 2026
$1.1M
NHLBI NIH HHS R01 HL174676NIDDK NIH HHS R01 DK106618
6 · The paper itself

Abstract

Primary aldosteronism is characterized by renin-independent hyperaldosteronism that originates from aldosterone-producing lesions in the adrenal glands. Under physiological conditions, aldosterone synthase ( Significance Statement: Primary aldosteronism is a common but under-diagnosed endocrine disease that contributes to global hypertension burden and cardiovascular mortality and morbidity. Hyperaldosteronism in primary aldosteronism is mainly caused by adrenal lesions harboring somatic mutations that disrupt intracellular calcium levels and consequently aldosterone synthase expression and aldosterone production. Majority of these mutations have been identified in genes encoding ion transporters/channels/pumps. Herein, we report the first disease-causing somatic mutations in human

Identifiers

PMID39484451
PMCPMC11526969

What Socratic 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 Socratic graph.