Research
Our Research
Our research program is focused on investigating immune cell and fibroblast crosstalk in the context of fibrosis and tissue repair by using high dimensional approaches and biomaterial platforms to interrogate the nature of their interactions during tissue fibrosis or tissue regeneration.
Our specific areas of interest are in pulmonary fibrosis, biomaterials-mediated fibrosis, and endometriosis and our goal is to identify key cell populations and signaling pathways that will enable the development novel diagnostic and therapeutic approaches for pulmonary fibrosis, as well as leverage existing biomaterial platforms in order to improve outcomes for biomaterials that are used clinically. Finally, our group engineers biomaterial-based human model system to study fibrotic disorders and identify new therapeutic strategies.
Our Mission
Our mission is to forge a vibrant and inclusive biomedical engineering research program that uniquely leverages synthetic biomaterials and high dimensional approaches to better understand the underlying mechanisms of fibrosis, a primary source of morbidity in numerous human diseases. These diseases include pulmonary fibrosis, liver cirrhosis, nephritis, macular degeneration, cardiovascular disease, endometriosis, and systemic scleroderma.
It has been reported that approximately 45% of deaths in the developed world can be attributed to fibrotic disorders. Despite the wide-reaching effects of fibrosis, the diversity of fibrotic disorders has made it difficult to identify their etiologies. We know fibrosis when we see it, but we do not know how it got there. Fibrosis is characterized by chronic inflammation followed by excessive myofibroblast accumulation and aberrant extracellular matrix (ECM) deposition. The chronic inflammatory component of fibrosis has been well characterized and even more so the myofibroblast and ECM components. However, there is a dearth of studies investigating how chronic inflammation leads to pathogenic fibroblast and ECM accumulation in fibrosis, as well as whether myofibroblasts contribute to perpetuate chronic inflammation