Related Experiment Video
Updated: Aug 11, 2026

Induction of Endothelial Differentiation in Cardiac Progenitor Cells Under Low Serum Conditions
Published on: January 7, 2019
A cardiac myocyte vascular endothelial growth factor paracrine pathway is required to maintain cardiac function
F J Giordano1, H P Gerber, S P Williams
1Cardiovascular Gene Therapy Program, Department of Medicine, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, Room 336C, New Haven, CT 06520, USA. Frank.Giordano@yale.edu
Insights
Cardiac myocytes are crucial for heart function, producing vascular endothelial growth factor (VEGF) essential for blood vessel formation and cardiac development. Deleting VEGF in these cells impairs heart structure and function.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Developmental Biology
Background:
- The role of cardiac myocytes in paracrine signaling within the heart is not fully understood.
- Investigating cardiomyocyte-derived secreted factors is crucial for understanding cardiac function and disease.
Purpose of the Study:
- To elucidate the role of cardiac myocyte-derived vascular endothelial growth factor (VEGF) in cardiac morphogenesis and function.
- To create a cardiomyocyte-specific knockout model for studying VEGF's impact on the heart.
Main Methods:
- Generated mice with cardiac myocyte-specific deletion of the vascular endothelial growth factor (VEGF) gene.
- Analyzed heart structure, microvessel density, contractile function, gene expression, and response to beta-adrenergic stimulation in knockout mice.
Main Results:
- Cardiac myocyte-specific VEGF deletion resulted in fewer coronary microvessels and thinned ventricular walls.
- Knockout hearts exhibited depressed basal contractile function and abnormal responses to beta-adrenergic stimulation.
- Hypoxia-responsive genes involved in energy metabolism were induced in knockout hearts.
Conclusions:
- Cardiac myocyte-derived VEGF is critical for cardiac morphogenesis and determining heart function.
- Established an adult murine model of hypovascular, nonnecrotic cardiac contractile dysfunction for further research.
Abstract:
The role of the cardiac myocyte as a mediator of paracrine signaling in the heart has remained unclear. To address this issue, we generated mice with cardiac myocyte-specific deletion of the vascular endothelial growth factor gene, thereby producing a cardiomyocyte-specific knockout of a secreted factor. The hearts of these mice had fewer coronary microvessels, thinned ventricular walls, depressed basal contractile function, induction of hypoxia-responsive genes involved in energy metabolism, and an abnormal response to beta-adrenergic stimulation. These findings establish the critical importance of cardiac myocyte-derived vascular endothelial growth factor in cardiac morphogenesis and determination of heart function. Further, they establish an adult murine model of hypovascular nonnecrotic cardiac contractile dysfunction.
Related Concept Videos
Paracrine Signaling
Mechanism of Angiogenesis
Regulation of Angiogenesis and Blood Supply
Structure of Cardiac Muscles
Compared to skeletal muscles, cardiac muscle cells are small and mostly have a single nucleus. Additionally, they are usually...
Pathophysiology of Cardiac Performance
Heart Failure II: Pathophysiology

