Key result
FGF20 overexpression protected against pressure overload-induced pathological cardiac hypertrophy and dysfunction by reducing oxidative stress through activation of the SIRT1 signaling pathway.
Why the study?
Sustained pathological cardiac hypertrophy can progress to heart failure, but the precise function of FGF20 in this process remains unclear.
Does FGF20 overexpression prevent pathological cardiac hypertrophy in preclinical models?
Does FGF20 overexpression prevent pathological cardiac hypertrophy in preclinical models?
p-value: p=<0.05
FGF20 protects against pathological cardiac hypertrophy by reducing oxidative stress through the SIRT1/FOXO1 signaling pathway, highlighting a potential novel therapeutic target.
Hypothesis-generating for FGF20-targeted therapy in hypertrophy; should not yet change clinical practice.
Cardiac hypertrophy occurs initially in response to an increased cardiac load as a compensatory mechanism to maintain cardiac output. However, sustained pathological hypertrophy can develop into heart failure and cause sudden death. Fibroblast growth factor 20 (FGF20) is a member of the fibroblast growth factor family, which involved in apoptosis, aging, inflammation, and autophagy. The precise function of FGF20 in pathological cardiac hypertrophy is unclear. In this study, we demonstrated that FGF20 was significantly decreased in response to hypertrophic stimulation. In contrast, overexpression of FGF20 protected against pressure overload-induced cardiac hypertrophy. Mechanistically, we found that FGF20 upregulates SIRT1 expression, causing deacetylation of FOXO1; this effect promotes the transcription of downstream antioxidant genes, thus inhibits oxidative stress. In content, the anti-hypertrophic effect of FGF20 was largely counteracted in SIRT1-knockout mice, accompanied by an increase in oxidative stress. In summary, our findings reveal a previously unknown protective effect of FGF20 on pathological cardiac hypertrophy by reducing oxidative stress through activation of the SIRT1 signaling pathway. FGF20 is a potential novel molecular target for preventing and treating pressure overload-induced myocardial injury.
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Chen et al. (2022) studied Pathological cardiac hypertrophy. FGF20 overexpression vs. Sham operation or empty vector was evaluated on Cardiac hypertrophy and dysfunction (p=<0.05). FGF20 overexpression protected against pressure overload-induced pathological cardiac hypertrophy and dysfunction by reducing oxidative stress through activation of the SIRT1 signaling pathway.
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