Heart failure & cardiomyopathies
Endothelial ZBTB16: a molecular shield against cardiac aging
Authors' conclusion
ZBTB16 preserves endothelial integrity and vascular niche homeostasis, protecting against aging-associated cardiac dysfunction. Its loss promotes EC senescence and fibrosis
Study context
- Population
- Aged human and mouse hearts; young mice with Zbtb16 deletion (Zbtb16-haploinsufficient and endothelial-specific knockout); senescent endothelial cell (ECs)
Main finding
As reported in the abstract
- Aged hearts: decreased chromatin accessibility and reduced ZBTB16 expression in humans and mice
- Zbtb16 deletion in young mice: premature aging, diastolic dysfunction, increased secretion of pro-fibrotic and inflammatory factors
- ZBTB16-deficient EC supernatants activated fibroblasts, induced cardiomyocyte hypertrophy, impaired neuronal sprouting
- ZBTB16 overexpression reversed these effects in senescent ECs and aged mice and reduced diastolic dysfunction
- ZBTB16 suppresses nuclear receptor-interacting protein 1, limiting fibroblast activation and pro-fibrotic signalling
Original publication
Endothelial ZBTB16: a molecular shield against cardiac aging. Eur Heart J. Published 6 January 2026. doi:10.
Summarised from the published abstract; every number is checked against it