Evidence map›Paper›PMID 41585488›Full record

ArticleiScience2026

The role of arachidonic acid metabolites in the subtype classification and pathogenesis of primary aldosteronism.

Mei You, Li Li, Xintao Tan, Xiaoli Liu, Lijuan Wang, Tingbing Cao, Bowen Wang, Min Liu, Yue Gao, Qing Zhou and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. 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

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

15 authors.

Mei YouDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Li LiDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Xintao TanDepartment of Urology, Daping Hospital, Army Medical University, Chongqing 400042, China.
Xiaoli LiuDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Lijuan WangDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Tingbing CaoDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Bowen WangDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Min LiuDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Yue GaoDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Qing ZhouDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Ruomei YangDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Weihua LanDepartment of Urology, Daping Hospital, Army Medical University, Chongqing 400042, China.
Peng GaoDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Zhiming ZhuDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.
Zhencheng YanDepartment of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Chongqing Key Laboratory of Metabolic Vascular Diseases, Daping Hospital, Army Medical University, Chongqing Institute of Hypertension, Chongqing 400042, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary aldosteronism (PA) is a common form of secondary hypertension with a complex diagnostic process and incompletely understood pathogenesis. In this controlled cross-sectional study, metabolomic profiling of 37 patients with bilateral PA, 38 with unilateral PA, and 20 with essential hypertension (EH) revealed that the most prominent metabolic difference lies in lipid metabolism, particularly arachidonic acid (AA) metabolism. We identified a panel of AA metabolites that improved PA subtyping. Additionally, levels of most AA metabolites were markedly reduced in PA patients after curative adrenal ablation. Mechanistically, treatment with AA enhanced the uptake of calcium ions and stimulated the proliferation and migration of adrenal cortical cells, with increased expressions of aldosterone synthase CYP11B2 and the calcium ion channel transient receptor potential canonical 3 (TRPC3). Furthermore, an inhibitor of TRPC3, pyr3, blocked these effects of AA. These findings elucidate the role of AA metabolites in PA pathogenesis and highlight them as potential targets for therapeutic intervention.

Indexed as

endocrinologymolecular biologyomicspharmacology

Identifiers

PMID41585488
PMCPMC12830227

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.