Inhibiting SHP2 improves ventricular remodeling by restoring AMPK phosphorylation and mitochondrial homeostasis
This study demonstrates that SHP2 acts as a key phosphatase directly dephosphorylates AMPK, thereby triggering mitochondrial dysfunction and exacerbating ventricular remodeling. Our findings provide novel mechanistic insights into heart failure progression and highlight SHP2 as a potential therapeutic target for heart failure treatment.
Authors
- Weiqi Li (ORCID: https://orcid.org/0000-0001-6141-1864)
- Huazhong Ying (ORCID: https://orcid.org/0000-0001-8502-8448)
- Xue Han (ORCID: https://orcid.org/0009-0009-4827-7678)
- Guang Liang (ORCID: https://orcid.org/0009-0005-1603-3223)
- Qiao-Juan Shi
- Yinyin Wu (ORCID: https://orcid.org/0009-0000-7107-4830)
- Meng Zhang (ORCID: https://orcid.org/0009-0004-5279-5164)
- Guo-Xuan Liu
- Ming-Yang He
- Ya-Nan Liu
- Jia-Ning Zheng
- Chen-Lu Liu
- Jie Tong
Institutions
- Zhejiang Provincial People's Hospital (CN)
- Hangzhou Medical College (CN)
Publication Details
- Journal
- Cell Communication and Signaling
- Published
- 2026-01-07
- DOI
- https://doi.org/10.1186/s12964-025-02620-2
- Primary Topic
- Protein Tyrosine Phosphatases
- Type
- article
- Field-Weighted Citation Impact
- 0.00