Tissue Repair and Regeneration

Nearly every disease, whether inflammatory, genetic, degenerative, metabolic, infectious, or otherwise, ultimately converges on a common problem: tissue damage. Yet tissues possess a remarkable capacity to rebuild. Our laboratory seeks to uncover the cellular and molecular principles that govern this process: how damaged tissues sense injury, mobilize immune and regenerative programs, and restore function. By understanding the fundamental biology of repair, we aim to identify new ways to regenerate tissues when healing fails and to restrain repair when it becomes pathological.

Our work has revealed that tissue repair is not simply an intrinsic property of damaged cells, but a coordinated dialogue between the immune system, tissue stem cells, and their surrounding environment. We discovered that the inflammatory cytokine IL-17 activates HIF-1α in injured epithelial cells, rewiring their metabolism toward glycolysis and providing the energy needed for cells to migrate and close a wound. This work uncovered an unexpected role for immune signals in helping damaged tissues adapt to the metabolic demands of injury and established a direct link between inflammation, metabolism, and regeneration.

We are now asking how other signals in the tissue environment shape the decision to repair. Emerging work from our laboratory explores how microbial products, including toxins typically associated with tissue injury, can paradoxically activate regenerative programs in the host. At the same time, we investigate what happens when repair loses its way, giving rise to pathological remodeling rather than restoration. By studying disorders such as intestinal fistulas, in which persistent injury and aberrant healing reshape tissue architecture, we hope to define the principles that separate successful regeneration from chronic disease and ultimately harness them to develop new regenerative therapies.