Key result
FGF20 prevents cardiac hypertrophy by inhibiting apoptosis and oxidative stress via ErbB2 activation.
Why the study?
FGF20 is involved in embryonic development and cardiac repair, but its role in cardiac hypertrophy and the underlying molecular mechanisms remained to be explored.
Does FGF20 prevent cardiac hypertrophy in preclinical models?
Does FGF20 prevent cardiac hypertrophy in preclinical models?
FGF20 prevents cardiac hypertrophy by inhibiting apoptosis and oxidative stress via activating ErbB2, suggesting a potential therapeutic target.
Hypothesis-generating in animal models; leaves open clinical translation of FGF20-ErbB2 targeting for hypertrophy.
Abstract Fibroblast growth factor 20 (FGF20) is a member of the fibroblast growth factor family and involved in embryonic development and cardiac repair. This study aimed to explore the role of FGF20 in cardiac hypertrophy and the underlying molecular mechanisms. FGF20 improved cardiac hypertrophy in vivo and in vitro. Furthermore, FGF20 increased expression of erythroblastic leukemia viral oncogene homolog 2 (ErbB2), which was negatively correlated with expression of the cardiac hypertrophy markers atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). In addition, FGF20 effectively protected cardiomyocytes against apoptosis and oxidative stress. To further investigate whether protective effect of FGF20 is mediated by ErbB2, neonatal rat cardiomyocytes (NRCMs) were treated with lapatinib, an inhibitor of ErbB2. Lapatinib largely abrogated the anti-hypertrophic effect of FGF20, accompanied by increases in cardiomyocyte apoptosis and oxidative stress. In summary, this study reveals that FGF20 prevents cardiac hypertrophy by inhibiting apoptosis and oxidative stress via activating ErbB2 and may be a promising therapeutic strategy for cardiac hypertrophy.
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Chen et al. (2024) studied Cardiac hypertrophy. Fibroblast growth factor 20 (FGF20) vs. Lapatinib (ErbB2 inhibitor) was evaluated on Cardiac hypertrophy, apoptosis, and oxidative stress. Fibroblast growth factor 20 prevented cardiac hypertrophy by inhibiting apoptosis and oxidative stress via activating ErbB2 in vivo and in vitro.
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