Sertad4 regulates pathological cardiac remodeling.
This study identifies Sertad4 as a fibroblast-enriched regulator of pathological cardiac remodeling that is upregulated in heart failure and myocardial infarction, demonstrating that its genetic deletion attenuates fibrosis, hypertrophy, and ventricular dysfunction, thereby suggesting it as a promising cell-type-selective therapeutic target to avoid the systemic toxicity associated with direct BRD4 inhibition.