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Updated: Jan 14, 2026
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Butein attenuates cardiac fibrosis by mediating TGF-β1/Smad signaling pathway after myocardial infarction
Mengmeng Deng1, Rui Ma2, Jinlei Li3
1Department of Cardiology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430000, Hubei Province, People's Republic of China.
Background:
Myocardial fibrosis has been found to accelerate heart dysfunction after myocardial infarction (MI). Butein is a chalcone compound possessing multiple biological properties. However, its effect on MI-induced myocardial fibrosis remains unclear.
Methods:
A mouse MI model was established by left anterior descending ligation. Human cardiac fibroblasts (HCFs) were stimulated with TGF-β1 in vitro. Mouse cardiac function was evaluated by assessing EF and FS. Masson's trichrome staining showed the fibrosis area in murine hearts. Western blotting evaluated protein levels of fibrosis markers and signaling-related markers. CCK-8, EdU, and Transwell assays were used to evaluate HCF proliferation and migration.
Results:
Butein improved MI-induced cardiac dysfunction and reduced the fibrosis area in mice. Butein inactivated TGF-β1/Smad signaling in MI mice and TGF-β1-stimulated HCFs. Butein inhibited TGF-β1-induced proliferation, migration, and collagen synthesis in HCFs, which were similar to the effects of LY2109761, a pharmacological inhibitor of TGF-β signaling.
Conclusion:
Butein mitigated MI development by inhibiting cardiac fibrosis and ECM deposition by inactivating the TGF-β1/Smad signaling pathway.
