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Updated: Jan 22, 2026

Complementation of Splicing Activity by a Galectin-3 - U1 snRNP Complex on Beads
Published on: December 9, 2020
Fibroblast growth factor 21 protects against pathological cardiac remodeling by modulating galectin-3 expression
Mengyao Sun1, Liying Jin1, Yang Bai1
1Department of Cardiac Surgery, first Hospital of Jilin University, Changchun, Jilin, P. R. China.
Background/Aims:
Fibroblast growth factor 21 (FGF21) plays a protective role in ischemia/reperfusion induced cardiac injury. However, the exact molecular mechanism of FGF21 action remains unclear. This study was designed the protective effect of FGF21 on the heart and its mechanism.
Method:
Adenovirus vector expressing FGF21 or control β-galactosidase was injected into the myocardium of mice. Myocardial injury was observed by tissue staining and immunohistochemical staining. The expression level of caspases-3 and galectin-3 in myocardial cells were observed by immunoblotting. Then, hypoxia-induced cell model was established. Small interfering RNA (SiRNA) and plasmid were transfected into H9c2 using Lipofectamine 2000 reagent (Invitrogen). The expression levels of galectin-3, ECM and cystatin-3 in cells were observed by immunoblotting, and the relationship between fibroblast growth factor 21 and galectin-3 was analyzed.
Result:
Cell test in vitro showed that FGF21 could inhibit apoptosis and decrease the expression of ECM (ColIaI, fibronectin, and alpha-SMA) under hypoxia. Western blot data showed that hypoxia-induced cell damage increased galectin-3 levels, while FGF21 decreased galactose lectin-3 levels. In addition, inhibition of galactose agglutinin-3 expression by siRNA enhanced the cardioprotective effect of FGF21, while overexpression of galectin-3 reduced the cardioprotective effect of fibroblast growth factor 21.
Conclusion:
FGF21 may be a novel therapy for hypoxia-induced cardiac injury by regulating the expression of galectin-3.
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