Junbing Chen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Junbing Chen has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Bing Han
Department of Cardiology, The First Hospital of Lanzhou University, Lanzhou, China
1 shared publication - Na Zhao
Department of Cardiology, Shaanxi Provincial People’s Hospital, Xi’an, China
1 shared publication - Shenghua Zhou
Department of Cardiology, The Second Xiangya Hospital of Central South University, Changsha, China
1 shared publication - Yongxiang Wang
Department of Cardiology, The First Hospital of Lanzhou University, Lanzhou, China
1 shared publication - Zhaowei Zhu
Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha
1 shared publication - Zheng Zhang
Department of Cardiology, The First Hospital of Lanzhou University, Lanzhou, China
1 shared publication
Latest Publications
- 30 October 2025
- Published by Springer Nature in Journal of Cardiovascular Translational Research
- Vol. 18 (5) , 1353-1370
PFKFB3 Promotes Myofibroblast Differentiation and Cardiac Fibrosis Through its Intra- and Extra- Cellular Roles
Cardiac fibrosis remains a major clinical challenge with limited therapeutic options, and the role of PFKFB3 in its pathogenesis remains unclear. Single-cell RNA sequencing analysis was applied and the results demonstrated that glycolysis was most prominently enhanced in activated cardiac myofibroblasts (myoCFs) in cardiomyopathy. Western blot analysis revealed that PFKFB3 expression was significantly increased in fibrotic hearts and TGF-β1-stimulated myoCFs. Genetic (Pfkfb3+/−) and pharmacological (3PO) inhibition of PFKFB3 attenuated myoCF activation, proliferation, and migration, while also reducing cardiac fibrosis in isoproterenol- and coronary ligation- induced mouse models. Mechanistically, TGF-β1 upregulated PFKFB3 in a HIF-1α-dependent manner, and extracellular PFKFB3 further promoted fibroblast activation and inflammatory responses. Clinically, elevated plasma PFKFB3 levels, as measured by ELISA, were significantly associated with fibrosis severity in patients with cardiomyopathy. These findings reveal for the first time that PFKFB3 drives cardiac fibrosis dually through intracellular glycolytic regulation and extracellular signaling, highlighting its translational potential. Graphical Abstract
- 30 October 2025
- Published by Springer Nature in Journal of Cardiovascular Translational Research
- Vol. 18 (5) , 1353-1370
PFKFB3 Promotes Myofibroblast Differentiation and Cardiac Fibrosis Through its Intra- and Extra- Cellular Roles
Cardiac fibrosis remains a major clinical challenge with limited therapeutic options, and the role of PFKFB3 in its pathogenesis remains unclear. Single-cell RNA sequencing analysis was applied and the results demonstrated that glycolysis was most prominently enhanced in activated cardiac myofibroblasts (myoCFs) in cardiomyopathy. Western blot analysis revealed that PFKFB3 expression was significantly increased in fibrotic hearts and TGF-β1-stimulated myoCFs. Genetic (Pfkfb3+/−) and pharmacological (3PO) inhibition of PFKFB3 attenuated myoCF activation, proliferation, and migration, while also reducing cardiac fibrosis in isoproterenol- and coronary ligation- induced mouse models. Mechanistically, TGF-β1 upregulated PFKFB3 in a HIF-1α-dependent manner, and extracellular PFKFB3 further promoted fibroblast activation and inflammatory responses. Clinically, elevated plasma PFKFB3 levels, as measured by ELISA, were significantly associated with fibrosis severity in patients with cardiomyopathy. These findings reveal for the first time that PFKFB3 drives cardiac fibrosis dually through intracellular glycolytic regulation and extracellular signaling, highlighting its translational potential. Graphical Abstract