Cardiac fibrosis is a key driver of heart disease, leading to stiffness and dysfunction due to excessive extracellular matrix deposition. Our lab investigates hot and cold fibrosis, two distinct fibrotic states. Hot fibrosis is inflammatory and dynamic, seen in acute injury, while cold fibrosis is stable and scar-like, common in chronic heart failure.
By studying these mechanisms, we aim to develop targeted therapies that modulate fibrosis, promote cardiac repair, and improve patient outcomes.