REST contributes to renal fibrosis through inducing mitochondrial energy metabolism imbalance in tubular epithelial cells
Our explorations revealed the upregulation of REST in renal fibrosis disrupts mitochondrial energy metabolism through transcriptionally suppressing OGDHL, which may act as a promising therapeutic target for renal fibrosis.
Authors
- Shaozong Qin
- Chun Zhou (ORCID: https://orcid.org/0000-0002-9257-468X)
- Shuiqin Gong (ORCID: https://orcid.org/0000-0002-9379-1424)
- Qigang Lan (ORCID: https://orcid.org/0000-0001-9697-9206)
- Jinghong Zhao (ORCID: https://orcid.org/0000-0001-9750-3285)
- Yinghui Huang (ORCID: https://orcid.org/0000-0002-9263-1111)
- Wenhao Liao (ORCID: https://orcid.org/0000-0002-6986-8663)
- Mengying Yao (ORCID: https://orcid.org/0000-0002-4203-1599)
- Yu Yang (ORCID: https://orcid.org/0000-0001-6884-5956)
- Wang Xin
Institutions
- Army Medical University (CN)
- Xinqiao Hospital (CN)
Publication Details
- Journal
- Cell Communication and Signaling
- Published
- 2025-04-08
- DOI
- https://doi.org/10.1186/s12964-025-02166-3
- Citations
- 10
- Primary Topic
- Birth, Development, and Health
- Type
- article
- Field-Weighted Citation Impact
- 34.94
Funders
- National Natural Science Foundation of China
- National Key Research and Development Program of China