Matthew S. Stratton

This study identifies Sertad4 as a fibroblast-specific regulator of cardiac fibrosis and remodeling, showing that its deletion reduces adverse outcomes after myocardial infarction.

This study shows BRD4 promotes cardiac fibrosis by dynamically targeting chromatin and activating gene expression in fibroblasts, revealing a signaling pathway involved in heart failure.

This study shows that HDAC11 suppresses thermogenic programs in adipose tissue via BRD2, leading to improved metabolic outcomes in HDAC11-deficient mice.