Mechanisms Underlying Myofibroblast Persistence in Fibrosis

Ascertain the mechanistic reasons for the persistence and continued activity of myofibroblasts in fibrotic tissues, including idiopathic pulmonary fibrosis, beyond normal wound healing resolution, to explain sustained extracellular matrix deposition and tissue stiffening.

Background

The authors emphasize that, under normal conditions, myofibroblasts undergo programmed cell death after wound closure, but in fibrotic diseases they remain active, producing excessive collagen and stiffening tissue.

Their paper proposes and investigates a contact-induced fibroblast-to-myofibroblast transition mechanism involving GqGPCR signaling and increased cytoskeletal tension, offering partial insight into persistence, while explicitly noting that the broader reasons for persistence are not well understood.