AP39 alleviates HHCY-induced myocardial remodeling by regulating FUNDC1-mediated mitochondrial dynamics via S-sulfhydration of NEDD8/CUL4B
These findings uncover a previously unrecognized mechanism by which AP39 preserves mitochondrial homeostasis through regulation of the FUNDC1-DRP1 axis via NEDD8/CUL4B-dependent S-sulfhydration. This study identifies a novel therapeutic target and provides mechanistic insight into HHCY-associated myocardial remodeling.
Authors
- Jie Yang (ORCID: https://orcid.org/0000-0003-4399-2532)
- Shengquan Liu (ORCID: https://orcid.org/0000-0002-8276-8333)
- Chenlong Luo
- Ting Yang (ORCID: https://orcid.org/0000-0002-7835-3899)
- X. Q. Yuan
- Chun Chu
- Yan Shi (ORCID: https://orcid.org/0000-0001-6140-9748)
- Yingchun Song
- Yaling Li
- Jianghe Jiang
- Xuan Li
Institutions
- Myocardial Solutions (United States) (US)
- First Affiliated Hospital of University of South China (CN)
- Artificial Intelligence in Medicine (Canada) (CA)
- University of South China (CN)
Publication Details
- Journal
- Frontiers in Pharmacology
- Published
- 2026-03-09
- DOI
- https://doi.org/10.3389/fphar.2026.1729145
- Primary Topic
- Folate and B Vitamins Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China