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Related Experiment Video

Updated: Dec 31, 2025

Light-sheet Fluorescence Microscopy to Capture 4-Dimensional Images of the Effects of Modulating Shear Stress on the Developing Zebrafish Heart
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Vezf1 regulates cardiac structure and contractile function.

Jere Paavola1, Tarja Alakoski2, Johanna Ulvila2

  • 1Unit of Cardiovascular Research, Minerva Foundation Institute for Medical Research, Helsinki, Finland.

Ebiomedicine
|January 9, 2020
PubMed
Summary

Vascular endothelial zinc finger 1 (Vezf1) is crucial for postnatal heart development and function. Reduced Vezf1 impacts cardiac growth and contraction, suggesting its role in human heart disease.

Keywords:
Cardiac contractile functionCardiac hypertrophyTEAD-1Vezf1

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology

Background:

  • Vascular endothelial zinc finger 1 (Vezf1) is a known regulator of blood vessel formation.
  • Its role in the postnatal heart remains largely unexplored.

Purpose of the Study:

  • To investigate the function of Vezf1 in postnatal cardiac development and contractile performance.
  • To elucidate the molecular mechanisms underlying Vezf1's cardiac regulation.

Main Methods:

  • Studied Vezf1's role in cardiac growth and function using zebrafish models and primary cardiomyocytes.
  • Analyzed gene expression, contractile responses, and protein interactions.

Main Results:

  • Vezf1 expression is downregulated in diseased human and mouse hearts.
  • Knockdown of Vezf1 in zebrafish impairs cardiac growth and contractile response to stimuli.
  • Vezf1 regulates genes associated with cardiac muscle contraction and dilated cardiomyopathy, targeting Myh7/β-MHC via an MCAT binding site.
  • TEAD-1 identified as a Vezf1 binding partner.

Conclusions:

  • Vezf1 plays a significant role in regulating compensatory cardiac growth and cardiomyocyte contractility.
  • These findings highlight Vezf1's potential relevance in the pathophysiology of human cardiac diseases.