Blocking immune cell biomechanical signals can reduce scar formation, providing a new target for antifibrotic therapy.

A research team at the University of Arizona recently revealed that a specific type of immune cell circulating in the blood plays a crucial role in the fibrosis process. By blocking the biomechanical signals emitted by these cells during wound healing, they can significantly reduce scar tissue formation and promote normal repair. This discovery provides a new potential strategy for preventing and treating fibrosis in multiple organs, including the lungs, liver, and heart.

Fibrosis is a pathological process of abnormal accumulation of scar tissue that can lead to organ failure and is associated with nearly half of all deaths in developed countries. There is currently no effective treatment approved by the FDA.

A research team published a paper in *Nature Biomedical Engineering* indicating that in the later stages of wound healing, a type of myeloid-derived immune cell senses mechanical signals and activates a pro-fibrotic pathway. When researchers interfered with this signal transduction in mouse models and in vitro human cells, the healing process shifted from scar formation to normal tissue repair, collagen arrangement became closer to healthy skin, and the function of anti-inflammatory cells was restored.

"We discovered a subset of circulating immune cells that is one of the major drivers of multi-organ fibrosis throughout the body," said Karen Chen, co-first author and associate professor of surgery at the University of Arizona, Tucson School of Medicine. "These cells are also highly expressed in human fibrotic skin and liver tissue."

This study further elucidates the interaction between mechanotransmission and immune regulation during the healing process. Dr. Jeffrey Gertner, Chair of the Department of Surgery, emphasized, "This discovery changes our understanding of fibrosis. Targeting those immune cells that sense mechanical stimuli, circulate in the body, and drive abnormal repair holds promise for preventing and even reversing fibrotic lesions in multiple organs."

Currently, the team is further exploring the regulatory mechanisms of related signaling pathways in order to promote the development of new intervention strategies for fibrosis.

source:

University of Arizona