The heart muscle cells (cardiomyocytes) constantly contract, which is essential for the heart to pump blood around the body. After an injury, such as a heart attack, millions of cardiomyocytes (CMs) are lost and cannot be innately restored due to the limited self-renewal ability. As a result, the heart remains unrepaired, forming scars (cardiac fibrosis), and undergoes progressive cardiac remodeling, which distorts the heart's structure and diminishes its function. These findings pose significant challenges in the treatment of heart failure.
We are working on developing therapeutic strategies to stimulate CM proliferation, reverse cardiac remodeling, reduce cardiac fibrosis, and improve cardiac function. To achieve this goal, we use technologies such as newly synthesized protein labeling and spatial transcriptomics to determine more comprehensive molecular mechanisms underlying cardiac injury and remodeling, including the Hippo and Wnt signaling pathways. We then develop gene therapy approaches to intervene in this process for the treatment of heart failure