Increased load leads to cardiac hypertrophy and endothelial cells play a vital role in maintaining oxygen supply to the heart through angiogenesis. However, insufficient angiogenesis contributes to the progression of heart failure. In our latest study, led by Elias Erny, we show that
– Endothelial cell proliferation declines as heart failure progresses, despite strong VEGF signaling.
– TCF19 and ATAD2 are key regulators of a gene program that is dysregulated at the transition from hypertrophy to heart failure.
– Knockdown of TCF19 and ATAD2 inhibits endothelial cell proliferation and angiogenesis.
– TCF19/ATAD2 levels and endothelial cell proliferation correlate in heart biopsies from patients with aortic stenosis
In conclusion, modifying downstream signaling pathways in endothelial cells rather than supplementing VEGF may be a way to improve cardiac angiogenesis and outcomes in patients with heart failure.
Erny et al. Basic Res Cardiol 2025