@article{Chen2026, 
author = {Jiang Chen and Shumin Yang and Xinyue Yang and Jiayu Li and Yifan He and Chuan Peng and Wei Zhang and Yi Yang and Junlong Li and Hongji Li and Furong He and Yong Xu and Wei Huang and Jinbo Hu and Qifu Li and Linqiang Ma},
title = {CXCR4 reduces aldosterone synthesis via regulating CYP11B2 expression},
year = {2026},
journal = {Genes & Diseases},
volume = {13},
number = {5},
keywords = {Aldosterone, Aldosterone-producing lesions, CXCR4, CYP11B2, ID3},
url = {https://www.sciopen.com/article/10.1016/j.gendis.2025.101956},
doi = {10.1016/j.gendis.2025.101956},
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 CYP11B2 transcription. Our data demonstrate that in aldosterone-producing lesions, CXCR4 expression is consistently elevated alongside CYP11B2, indicating a potential compensatory mechanism to counteract elevated aldosterone levels.}
}