About the Lab
Our lab focuses on studying cellular and molecular mechanisms leading to cardiac dysfunction with aging.
Within the last decade, we discovered that the fibroblasts isolated from the old mouse heart have an altered phenotype compared with those from young hearts. In the old heart, fibroblasts become more activated and secrete higher levels of various extracellular matrix components (such as various collagen types and fibronectin containing extra domain A) and inflammatory cytokines such as MCP-1, CX3CL1 and IL-6.
As they produce more matrix components, the heart becomes more fibrotic, which directly leads to diastolic dysfunction. Because of inflammatory chemokines, leukocytes from the blood are chemoattracted into the heart. In the aging heart environment, some of the infiltrating monocytes polarize into pro-fibrotic or pro-inflammatory macrophages.
The lab also examines the possible therapeutic approaches to correct defective pathways and “normalize” pathological phenotypes, and thereby prevent further deterioration of cardiac function.