Why the study?
LVH is associated with increased cardiac FGF23 expression in mice and men, but the specific role of cardiac FGF23 in LVH required further elucidation.
Does cardiomyocyte-specific deletion of Fgf23 improve cardiac metabolic health and reduce hypertrophy or fibrosis in a mouse model of pressure overload-induced LVH?
Population
Mice subjected to transverse aortic constriction and cultured cardiomyocytes
Comparison
Cardiomyocyte-specific Fgf23 knock-out vs Fgf23 fl/fl controls
Design
Preclinical animal and cell-culture experimental study
Key result
Cardiomyocyte-specific deletion of Fgf23 in mice subjected to pressure overload ameliorated hypertension and cardiac fibrosis, and induced a metabolic switch downregulating glucose consumption.
Authors
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Hypothesis-generating for cardiac FGF23 inhibition in pressure overload; leaves open human translation.
Does cardiomyocyte-specific deletion of Fgf23 improve cardiac metabolic health and reduce hypertrophy or fibrosis in a mouse model of pressure overload-induced LVH?
Deletion of cardiac FGF23 in a mouse model of pressure overload ameliorates hypertension and cardiac fibrosis by shifting myocardial energy metabolism from glucose consumption to fatty acid oxidation, mimicking the cardioprotective effects of SGLT2 inhibitors.
Latic et al. (2025) studied Left ventricular hypertrophy. Cardiomyocyte-specific Fgf23 deletion vs. Fgf23fl/fl control mice was evaluated on Development of left ventricular hypertrophy, cardiac fibrosis, and myocardial energy metabolism. Cardiomyocyte-specific deletion of Fgf23 in mice subjected to pressure overload ameliorated hypertension and cardiac fibrosis, and induced a metabolic switch downregulating glucose consumption.