Fibroblast growth factor-2 mediates pressure-induced hypertrophic response

Area of Science:

• Cardiology
• Molecular Biology
• Physiology

Background:

• Fibroblast growth factor-2 (FGF2) is linked to cardiomyocyte growth in vitro.
• Its in vivo role in pressure-induced cardiac hypertrophy is not well understood.

Purpose of the Study:

• To investigate the in vivo role of FGF2 in cardiac hypertrophy induced by pressure overload.

Main Methods:

• Mice with or without FGF2 underwent transverse aortic coarctation (AC).
• Echocardiography assessed left ventricular (LV) mass and wall thickness.
• In vivo LV function, cardiomyocyte size, and fetal gene expression were measured.

Main Results:

• AC Fgf2(-/-) mice showed significantly less cardiac hypertrophy compared to AC Fgf2(+/+) mice.
• Cardiomyocyte size was reduced, and beta-adrenergic responses were preserved in AC Fgf2(-/-) mice.
• Myosin heavy chain composition depended on hemodynamic stress, not FGF2 or hypertrophy.

Conclusions:

• FGF2 plays a major role in cardiac hypertrophy during pressure overload.
• FGF2 deficiency attenuates hypertrophy and preserves cardiac function.
• Myosin heavy chain isoform switching is transcriptionally regulated by hemodynamic stress.