Proteomic study on the protective mechanism of fibroblast growth factor 21 to ischemia-reperfusion injury
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Updated: May 7, 2026
Isolation and Characterization of Adult Cardiac Fibroblasts and Myofibroblasts
Published on: March 12, 2020
Wei-Tao Cong1, Jin Ling, Hai-Shan Tian
1a Zhejiang Provincial Key Laboratory of Biopharmaceuticals, Wenzhou Medical College, Wenzhou, Zhejiang 325035, P.R. China.
Abstract:
Fibroblast growth factor (FGF)-21 is a novel regulator of insulin-independent glucose transport in 3T3-L1 adipocytes and has glucose and triglyceride lowering effects in rodent models of diabetes. In this study, we found that FGF-21 can significantly attenuate ischemia-reperfusion (I/R) induced damage in H9c2 cells (rat heart). However, it is unclear which signal transduction pathway is involved in the cardioprotective effect of FGF-21. Thus, this study was designed to investigate the potential mechanism induced by FGF-21. The results showed that FGF-21 treatment prevented the oxidative stress and apoptosis associated with I/R damage by reducing the levels of superoxide anions, inhibiting glycogen synthase kinase (GSK) 3β by activating Akt phosphorylation, and recovering the levels of ATP synthase pyruvate kinase isozymes M1 and protein kinase C, thereby improving energy supply. In summary, we conclude that FGF-21 protects H9c2 cells against I/R injury mainly through the Akt-GSK-3β-caspase-3 dependent pathway, preventing oxidative stress, and recovery of the energy supply.
Insights
Fibroblast growth factor (FGF)-21 protects rat heart cells from ischemia-reperfusion injury. FGF-21 reduces oxidative stress and apoptosis via the Akt-GSK-3β pathway, improving cellular energy supply.
Area of Science:
- Cardiovascular Research
- Cellular Biology
- Endocrinology
Background:
- Fibroblast growth factor (FGF)-21 regulates glucose transport and has lipid-lowering effects.
- FGF-21 demonstrates potential cardioprotective effects against ischemia-reperfusion (I/R) injury.
- The specific molecular mechanisms underlying FGF-21's cardioprotection remain largely unknown.
Purpose of the Study:
- To elucidate the signal transduction pathway involved in FGF-21's protective effects against I/R injury in cardiac cells.
- To investigate how FGF-21 mitigates oxidative stress and apoptosis during I/R.
- To determine FGF-21's role in maintaining cellular energy supply under I/R conditions.
Main Methods:
- Utilized H9c2 cells (rat heart-derived cell line) to model I/R injury.
- Assessed oxidative stress markers, including superoxide anion levels.
- Investigated the involvement of the Akt-GSK-3β signaling pathway and apoptosis markers.
- Measured ATP synthase, pyruvate kinase isozymes M1, and protein kinase C levels to evaluate energy supply.
Main Results:
- FGF-21 treatment significantly attenuated I/R-induced damage in H9c2 cells.
- FGF-21 reduced oxidative stress and apoptosis by inhibiting glycogen synthase kinase (GSK) 3β through Akt phosphorylation.
- FGF-21 treatment restored cellular energy supply by recovering levels of ATP synthase, pyruvate kinase isozymes M1, and protein kinase C.
Conclusions:
- FGF-21 confers cardioprotection against I/R injury in H9c2 cells.
- The protective mechanism involves the Akt-GSK-3β-caspase-3 dependent pathway, mitigating oxidative stress.
- FGF-21 enhances cellular energy supply, contributing to its protective role in I/R injury.
