ATF4 promotes renal tubulointerstitial fibrosis through hexokinase II-mediated glycolysis
In this study, we identified a marked induction of tubular ATF4 in mice subjected to UUO. Silencing ATF4 significantly mitigated renal tubulointerstitial fibrosis. Mechanistically, ATF4 was shown to act as a key glycolytic driver by transcriptionally upregulating hexokinase II. Collectively, these findings indicate that tubular ATF4 facilitates renal tubulointerstitial fibrosis through HK-II mediated glycolytic activation.
Authors
- Zuo‐Lin Li (ORCID: https://orcid.org/0000-0002-6694-8406)
- Songtao Feng (ORCID: https://orcid.org/0000-0002-7773-5406)
- Yan Zhou (ORCID: https://orcid.org/0000-0001-6685-2634)
- Yue-Ming Gao (ORCID: https://orcid.org/0000-0001-5640-3966)
- Wei‐Jie Ni
- Hui Qian
- Zheng Wang (ORCID: https://orcid.org/0000-0002-0490-466X)
- Junbo Ge (ORCID: https://orcid.org/0000-0002-9360-7332)
- Lu Sun (ORCID: https://orcid.org/0000-0003-2393-241X)
- Mingyue Yuan (ORCID: https://orcid.org/0000-0002-1331-5373)
- Bi-Cheng Liu (ORCID: https://orcid.org/0000-0002-9220-0477)
Institutions
- Jiangsu University (CN)
- Peking University (CN)
- Zhongda Hospital Southeast University (CN)
- Affiliated Hospital of Jiangsu University (CN)
- Peking University Third Hospital (CN)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2025-12-17
- DOI
- https://doi.org/10.3389/fimmu.2025.1683249
- Citations
- 1
- Primary Topic
- Chronic Kidney Disease and Diabetes
- Type
- article
- Field-Weighted Citation Impact
- 1.43