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Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
Published on: September 25, 2017
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FGF23/FGFR4-mediated left ventricular hypertrophy is reversible.
Alexander Grabner1,2, Karla Schramm1,3, Neerupma Silswal4
1Katz Family Drug Discovery Center and Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA.
Scientific Reports
|May 18, 2017
Summary
Fibroblast growth factor 23 (FGF23) causes cardiac hypertrophy, but this effect is reversible. Blocking FGF receptor 4 (FGFR4) reduces left ventricular hypertrophy in chronic kidney disease and aging models.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Nephrology
Background:
- Fibroblast growth factor 23 (FGF23) is a hormone linked to cardiac dysfunction in chronic kidney disease (CKD).
- FGF23 targets cardiac myocytes via FGF receptor 4 (FGFR4), promoting left ventricular hypertrophy (LVH).
- The reversibility of FGF23-induced cardiac effects and its role in aging-related cardiac remodeling are unclear.
Purpose of the Study:
- To investigate the reversibility of FGF23-induced cardiac hypertrophy.
- To determine the role of FGFR4 in CKD- and age-related LVH.
- To explore the therapeutic potential of targeting FGF23/FGFR4 signaling in cardiac remodeling.
Main Methods:
- In vitro and in vivo studies of FGF23-induced cardiac hypertrophy.
- Utilizing the 5/6 nephrectomy rat model for CKD-induced LVH.
- Employing aging mice and FGFR4 knockout mice to study age-related cardiac remodeling.
- Assessing cardiac contractility and aortic relaxation.
Main Results:
- FGF23-induced cardiac hypertrophy was reversible upon removal of the stimulus.
- Specific blockade of FGFR4 attenuated established LVH in CKD rats.
- Aging mice lacking FGFR4 were protected from LVH.
- FGF23 increased cardiac contractility through FGFR4.
Conclusions:
- FGF23/FGFR4 signaling plays a significant role in regulating cardiac remodeling and function.
- Targeting cardiac FGF23/FGFR4 signaling may offer a protective strategy against CKD- and age-related LVH.
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