PINK1 modulates Prdx2 to reduce lipotoxicity‐induced apoptosis and attenuate cardiac dysfunction in heart failure mice with a preserved ejection fraction
Our investigation discloses a pivotal relationship between PINK1 and Prdx2 in the context of HFpEF. Notably, PINK1, in addition to its role in mitochondrial autophagy, can increase Prdx2 expression, effectively remove ROS and attenuate cardiomyocyte apoptosis by modulating the JNK and p38 pathways, thereby alleviating myocardial lipotoxicity and improving HFpEF cardiac function. Our studies offer valuable insights, opening avenues for the development of innovative therapeutic strategies in the prevention and treatment of HFpEF.
Authors
- Dingli Xu
- Xiyuan Mei
- Haobin Zhou (ORCID: https://orcid.org/0000-0002-8905-3584)
- Zeng Qingchun
- Zhuang Ma (ORCID: https://orcid.org/0000-0002-7286-1155)
- Qiming Zhao (ORCID: https://orcid.org/0009-0005-1463-5829)
- Tianyu Xu (ORCID: https://orcid.org/0000-0002-2929-6760)
- Xianghui Zeng (ORCID: https://orcid.org/0000-0002-9372-1063)
- Qiling Yang
- Hao Ren
- Hao Zhang (ORCID: https://orcid.org/0000-0002-9192-4684)
Institutions
- Ministry of Education of the People's Republic of China (CN)
- Sun Yat-sen University (CN)
- Nanfang Hospital (CN)
- The First Affiliated Hospital, Sun Yat-sen University (CN)
- Southern Medical University (CN)
Publication Details
- Journal
- Clinical and Translational Medicine
- Published
- 2025-01-01
- DOI
- https://doi.org/10.1002/ctm2.70166
- Citations
- 5
- Primary Topic
- Redox biology and oxidative stress
- Type
- article
- Field-Weighted Citation Impact
- 4.03
Funders
- National Natural Science Foundation of China