Program Leaders
Following injury, dynamic repair programs shape whether tissues regenerate, resolve injury, or progress toward persistent scarring. This balance can be disrupted by aging, chronic inflammation, or disease, where normal healing can transition into fibrosis — a progressive process marked by excessive extracellular matrix deposition, tissue stiffening, and loss of organ function. Fibrosis contributes to disease in nearly every major organ system and remains difficult to reverse once established. Thus, understanding the early cellular and matrix-driven events that tip tissues away from regeneration and toward chronic remodeling is critical for developing new regenerative therapies.
The IRM Program in Fibrosis, Cell Matrix, and Regeneration brings together interdisciplinary investigators who study how cells create, sense, and remodel their extracellular matrix during development, homeostasis, injury, and disease. Program members combine expertise in stem and progenitor cell biology, matrix biology, mechanobiology, inflammation, biomaterials, organoids, tissue engineering, and clinical models of fibrotic disease. Together, we seek to define the mechanisms that govern regenerative versus fibrotic outcomes and to develop new therapeutic strategies that interrupt pathological scarring, restore healthy tissue architecture, and promote functional regeneration.
The program also serves as a collaborative hub for the IRM community by supporting shared infrastructure, educational initiatives, and new cross-disciplinary partnerships. Through a virtual core focused on fibrosis, matrix biology, and regenerative models, the program aims to connect investigators with relevant tools, assays, expertise, and model systems. Educational activities, including seminars, workshops, trainee-focused programming, and thematic symposia, foster interaction across basic, engineering, and clinical research communities and train the next generation of scientists working at the interface of fibrosis, cell–matrix biology, and regeneration.