Approximately six million Americans suffer from poor cutaneous wound healing (e.g. diabetic wounds, pressure wounds) annually, with 1.1 to 1.8 million new cases arising each year. It is estimated that we spend over $20 billion annually in wound care for these patients. Further, fibroses throughout the body are estimated to be responsible for 45% of all deaths in the U.S. Fibrosis can develop in any organ, often with devastating effects. Of patients who undergo abdominal surgery, 93% will develop abdominal adhesions, or bands of fibrous tissue that form between organs and the abdominal wall. From 1998 to 2002, 18.1% of hospitalizations were related to abdominal adhesions, resulting in an estimated cost of $1.18 billion annually. Unfortunately, there are limited means to prevent or treat fibroses such as scars and adhesions, or their sequelae.

​

We hope to characterize and develop therapies to minimize and even prevent the development of scar tissue that develops in the skin, abdomen, and other sites, thereby addressing the clinical and financial burdens related to wound healing and fibrosis.

​

We currently have projects in the following areas, and collaborate with other laboratories to develop and test novel small molecule therapies, three-dimensional hydrogels to deliver cells and therapies, and disease models:

​

1.     Pathophysiology of abdominal adhesion formation.

2.     Identification and characterization of dermal lineages critical for fibrosis and scar formation in dorsal and ventral skin.

3.     The effect of small molecule inhibitors on cutaneous wound repair and regeneration.

4.     The role of the nervous system in wound repair, regeneration, and fibrosis. 

5.     The role of creeping fat in intestinal fibrosis. 

 

6.      Molecular mechanisms of repair in mouse models of wound regeneration (e.g., fetal wound repair).

7.      Adipocyte dynamics and plasticity in cutaneous tissue repair.

8.      Idiopathic pulmonary fibrosis (IPF) is a progressive and often terminal illness that affects over 5 million people around the world, with an average survival time of less than 4 years after diagnosis. Fibroblasts have been implicated in fibrotic matrix deposition in the lungs, but the impact of specific subpopulations on fibrosis and tissue remodeling is unclear. Ultimately, there is a significant clinical demand for biological therapies that can promote remodeling and repair of lungs impacted by IPF. We are investigating the contributions of fibroblasts, other pulmonary cell types, and extracellular matrix morphology to dynamic biological processes during IPF progression and remodeling. Using mouse models and clinical data, we are uncovering specific cellular populations and signaling pathways that may be modulated to promote the repair of fibrotic lungs.