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Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
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A human cell atlas of the pressure-induced hypertrophic heart

Luka Nicin1,2,3, Sam Michael Schroeter1,2,3, Simone Franziska Glaser1,2,3

  • 1Institute for Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt, Germany.

Nature Cardiovascular Research
|August 28, 2024
PubMed

Insights

This study reveals how pressure overload alters heart cells in aortic valve stenosis. Reduced communication between endothelial cells and cardiomyocytes impairs heart function, highlighting intercellular crosstalk

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Crosstalk in Heart Disease

Background:

  • Pathological cardiac hypertrophy is a major cause of heart failure.
  • A comprehensive understanding of cellular and gene expression changes in the human hypertrophic heart is lacking.

Purpose of the Study:

  • To investigate the transcriptional response of human cardiomyocytes to pressure overload.
  • To identify alterations in cardiac cellular crosstalk during pathological cardiac hypertrophy.

Main Methods:

  • Large-scale single-nucleus transcriptomics was employed to analyze human heart tissue.
  • In vitro experiments were conducted to assess the functional role of specific molecular interactions.

Main Results:

  • Significant downregulation of Eph receptor tyrosine kinases, including EPHB1, was observed in hypertrophied cardiomyocytes.
  • Reduced EPHB1 activation due to decreased ephrin (EFN)B2 expression from endothelial cells was noted.
  • Endothelial cell-derived EFNB2 demonstrated an inhibitory effect on cardiomyocyte hypertrophy in vitro.

Conclusions:

  • Intercellular crosstalk is crucial in the pathogenesis of cardiac hypertrophy and heart failure.
  • The study provides a valuable human cell atlas of the hypertrophied heart.
  • Targeting the EPHB1-ephrinB2 pathway may offer therapeutic potential for heart failure.

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