ZBTB16 as a key factor for cardiac aging and disease
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Technology
Scientists from the Goethe University Frankfurt, in particular from the Institute of Cardiovascular Regeneration, have identified ZBTB16 as a master regulator of endothelial integrity and vascular niche homeostasis in the
aging heart.
Reduced ZBTB16 expression promotes endothelial senescence, impairs angiogenic function and triggers pro-fibrotic signaling. Increasing its expression in endothelial cells counteracts these effects and improves cardiac function in aged mice.
The underlying mechanism involves suppression of NRIP1, a downstream target associated with fibroblast activation and pro-fibrotic signaling.
Application
The technology offers a potential approach to preventing and treating age-related cardiac dysfunction, particularly diastolic dysfunction and fibrotic remodeling.
By preserving endothelial function and communication between cells in the cardiac microenvironment, targeting ZBTB16 could enable intervention early in the disease process rather than only addressing downstream effects.
Technology stage
The project has reached preclinical proof of concept, with evidence from in vitro studies and aged mouse models in vivo.
Endothelial overexpression of ZBTB16 using targeted AAV9 vectors has shown beneficial effects on cardiac function in aged mice. Initial exploratory experiments also suggest that ZBTB16 expression may be pharmacologically inducible, providing a potential route for further therapeutic development.
