Published in Cell

Talk Abstract

Fibrosis, or scarring, is the pathologic accumulation of excess ECM that affects nearly every tissue and is implicated in 45% of all deaths in the industrialized world. In adult mammals, a deep skin wound heals by forming a fibrotic scar that lacks dermal appendages (hair follicles, glands), contains dense, misaligned ECM fibers, has increased cellularity, and can be chronically inflamed. This results in permanent loss of skin function such as thermoregulation, disfigurement, growth restriction, and chronic disability due to intractable pain and itch. The absence of effective treatments to restore skin function following injury is because of our limited understanding of mechanisms that prevent, or promote, skin regeneration. In this public seminar, Sarthak Sinha, an MD/PhD candidate in Dr. Jeff Biernaskie’s Lab at the University of Calgary, highlights that although dermal fibroblasts typically acquire fibrotic fates by secreting inflammatory signals that intensify the reparative immune response, they harbour a latent capacity to reactivate developmental programs to support skin regeneration. Their recent studies in small and large mammalian models of wound healing suggest fibroblasts function at the nexus of tissue repair and inflammation as their secretome amplifies effector immune programs at the expense of tissue function and highlights stromal-immune crosstalk neutralization as a promising anti-fibrotic therapy.