Evidence map›Paper›PMID 42290661›Full record

ArticleGenes & diseases2026

CXCR4 reduces aldosterone synthesis via regulating CYP11B2 expression.

Jiang Chen, Shumin Yang, Xinyue Yang, Jiayu Li, Yifan He, Chuan Peng, Wei Zhang, Yi Yang, Junlong Li, Hongji Li and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

16 authors.

Jiang ChenDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Shumin YangDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Xinyue YangDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Jiayu LiDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Yifan HeDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Chuan PengDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Wei ZhangDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Yi YangDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Junlong LiDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Hongji LiDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Furong HeDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Yong XuDepartment of Endocrinology and Metabolism, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China.
Wei HuangDepartment of Endocrinology and Metabolism, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China.
Jinbo HuDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Qifu LiDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Linqiang MaDepartment of Endocrinology, Sichuan-Chongqing Joint Key Laboratory of Metabolic Vascular Diseases, Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C-X-C motif chemokine receptor 4 (CXCR4) is highly expressed in aldosterone-producing adenoma, and gallium-68 pentixafor PET-CT imaging targeting CXCR4 has been utilized for subtype diagnosis in primary aldosteronism. However, the roles of CXCR4 in regulating aldosterone biosynthesis remain poorly understood. In this study, we observed a strong co-localization of aldosterone synthase (CYP11B2) and CXCR4 in aldosterone-producing adenoma and other aldosterone-producing lesions. Functional experiments in H295R cells revealed that CXCR4 overexpression significantly suppressed both aldosterone synthesis and CYP11B2 expression, whereas CXCR4 knockdown conversely enhanced aldosterone production and up-regulated CYP11B2. Mechanistically, CXCR4 inhibited aldosterone biosynthesis by up-regulating inhibitor of DNA binding (ID) proteins, which directly repressed

Indexed as

AldosteroneAldosterone-producing lesionsCXCR4CYP11B2ID3

Identifiers

PMID42290661
PMCPMC13264065

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