Endothelial p53 deletion prevents cardiac fibrosis and heart failure in a mouse model of pressure overload, suggesting endothelial cells as a potential therapeutic target for preserving cardiac function during hypertrophy.
Our analyses reveal that accumulation of p53 in endothelial cells contributes to blood vessel rarefaction and fibrosis during chronic cardiac pressure overload and suggest that endothelial cells may be a therapeutic target for preserving cardiac function during hypertrophy.
Gogiraju et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: