Histone Lactylation Promotes Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure by Regulating TGFB2 Expression
Histone lactylation promotes pathological cardiac hypertrophy and heart failure by upregulating TGFB2 and activating PI3K/AKT/mTOR signaling. These findings identify histone lactylation as an epigenetic link between metabolic reprogramming and hypertrophic signaling, and suggest it as a potential therapeutic target for pathological cardiac remodeling.
Authors
- Hongfei Xu (ORCID: https://orcid.org/0000-0002-8891-2463)
- Weidong Li (ORCID: https://orcid.org/0000-0002-8395-7216)
- Yong Cui (ORCID: https://orcid.org/0000-0003-1934-0809)
- Peng Teng (ORCID: https://orcid.org/0000-0002-7412-9646)
- Jing Li (ORCID: https://orcid.org/0000-0003-1191-9971)
- Miao Chen
- Zhen Wang (ORCID: https://orcid.org/0000-0001-9289-4889)
- Liang Ma (ORCID: https://orcid.org/0000-0001-8054-4582)
- Yinze Wei
Institutions
- The Fourth People's Hospital (CN)
- Zhejiang Provincial People's Hospital (CN)
- First Affiliated Hospital Zhejiang University (CN)
Publication Details
- Journal
- Circulation Research
- Published
- 2025-12-11
- DOI
- https://doi.org/10.1161/circresaha.125.326185
- Primary Topic
- Cardiac Fibrosis and Remodeling
- Type
- article
- Field-Weighted Citation Impact
- 0.00