BACH1 deficiency improves placental angiogenesis via SLC25A51-mediated mitochondrial NAD+ transport in intrahepatic cholestasis of pregnancy
BACH1 may suppress placental angiogenesis by inhibiting the transcriptional expression of SLC25A51, making it a potential therapeutic target. Specifically, pharmacological inhibition of BACH1 could provide a targeted therapeutic strategy for placental angiogenesis associated with ICP.
Authors
- Shengpeng Li (ORCID: https://orcid.org/0009-0006-5018-4380)
- Huimin Zhao (ORCID: https://orcid.org/0000-0002-9069-6739)
- Ling Ai
- Wei-ying Zhu
- Yanli Zhang (ORCID: https://orcid.org/0000-0003-1481-6361)
- Wenlong Zhang (ORCID: https://orcid.org/0000-0001-7013-7668)
- Yaxian Wu (ORCID: https://orcid.org/0009-0001-6879-7621)
- Jiaojiao Sun
- Dan Chen
- Qingfeng Pang
- Z. Z. Xing (ORCID: https://orcid.org/0009-0003-1340-4370)
Institutions
- Jiangnan University (CN)
- Jiaxing University (CN)
- First Hospital of Jiaxing (CN)
Publication Details
- Journal
- Molecular Medicine
- Published
- 2025-05-01
- DOI
- https://doi.org/10.1186/s10020-025-01215-4
- Citations
- 2
- Primary Topic
- Drug Transport and Resistance Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 2.09
Funders
- Government of Jiangsu Province
- Jiangnan University